All molecules have a 3D shape. This is referred to as it's conformation. Most molecules have certain degrees of flexibility. For example, single bonds usually allow free rotation, while double bonds don't. Cyclic structures have less freedom, but can still twist into several shapes. This can be important because some molecules bend into a certain conformation and then fit into protein binding sites they normally couldn't fit into. And it's not just small molecules, proteins, RNA, and DNA fold into specific shapes, and often must be unfolded, twisted, or bent in order to carry out their function. Protein dynamics is an active field of study. A great example is the ATP synthetase, which has a large rotating portion and acts a lot like a motor.


Are there any examples of how to apply evolutionary models?

Hypothesis testing in evolutionary biology

Pretty much any paper of empirical evolutionary biology tests hypothesis. If you go on google scholar and look for any empirical paper in the field of evolutionary biology such as "does sexual selection has antagonist effect to natural selection", "evolution of range limits", "evolution of mutational robustness" or "sensory drive speciation" you will find tons of papers that test hypotheses. Many of these hypotheses have been developed either in pure theory papers on in papers that mix some level of theory (no necessary need of complicated modelling) and empirical work. There is nothing in evolutionary biology that is different from the other field of biology or the other fields of science in our ability to test hypotheses.

A tiny bit of history

In the first half of the century most work in evolutionary biology was theoretic. Many hypotheses were left untested. Today, we perform lots of tests and the technics of molecular genetics (sequencing and stuff) help a lot to test hypotheses. Some papers, indeed uses metrics that are very hard to estimate, eventually too hard (too expensive) to be estimated today, it is true and it is an issue, an issue that all sciences know of. We sometimes have to wait for technical advancements before being able to test a hypothesis.

Concerning the paper you mention

From your description of the work they performed in the paper you linked (I haven't read this paper) it sounds like they are describing the concept of shifting balance theory, a process that has been first hypothesize by S. Wrigth in 1932. As said on the wiki article, there is little empirical evidence for shifting balance theory (but you may want to read this and that). The reason is that shifting balance theory is link to the concept of adaptive landscape. Adaptive landscape is what we call the relationship between fitness and phenotype or fitness and genotype. We have descriptions of fitness-phenotype relationship but we are only starting to offer good and complete descriptions fitness-phenotype-genotype relationship. Understanding the link between genotype and fitness is essential for testing shifting balance theory. Shifting balance theory is a logical consequence of the process of drift and selection, both of which are very well known (and well tested). Most of the issue is in the description of how rough is the fitness landscape to know whether shifting balance theory is indeed a thing that occurs in nature or whether it is very unlikely of such process to ever occur.


How does boiling water release dyes from vegetables?

Why boiling water releases dyes from vegetables:

In general, one would need a solvent to extract compounds from the vegetables. Water is a solvent for the coloured pigments. In air or oil, the same pigments are less or even not at all soluble.
Hot water can damage cells. Proteins, which give structure to cells and membranes, denature at hot temperatures. Cell walls, by the way, are much more robust than membranes.
But even in cold water, some pigments can pass through membranes or membrane channels by diffusion. This will only take more time.

There are possibly other factors that are more case (vegetable) specific.


Why even if all requirements for natural selection are met, it may not happen?

Evolution, a change in the trait distribution of a population, occurs by four mechanisms; drift, mutation, migration, and selection. E.g. These mechanisms cause a change in the mean of trait, or variance in a trait etc.. Just to summarise the conditions you gave:

a) Trait $i$ has variation

b) Trait $i$ covaries with fitness ($\omega$)

c) Trait $i$ is heritable from parent to offspring

Genetic drift is the random loss of genetic variance from the population by stochastic processes. Mutation (generally) generates new genetic variation within populations. Migration can lead to loss (emigration) or gain (immigration) of genetic variation from a population, as variants come or go from a population.

Selection is mechanism underlying adaptation. This is what is in condition b of the conditions you gave. We can predict the response to selection using some simple quantitative genetics in the form of the (multivariate) breeders equation.

$\Delta z = G\beta$

Where $\Delta z$ is the response in the trait, $G$ is the genetic (co)variance matrix, and $\beta$ is the selection.

In a simple toy example we could look at a single trait, $i$. We allow $i$ to satisfy all of the above conditions. This means that both $G$ and $\beta$ are non-zero, and therefore, $\Delta z_i$ will also be non-zero. Just putting some random numbers in to the equation to make it clear, if $G = 0.5$ and $\beta = 0.8$ then;

$\Delta z_i = 0.5 \times 0.8 = 0.4$

Mutation, drift, and migration could all oppose or distort the effect of selection. In other words, they can cause the actual and predicted response to be different from one another (i.e. $\Delta z_i \neq 0.4$), and there will not necessarily be a change in the phenotypic distribution.

However, selection is also factor that could cause a difference between the predicted and actual response to selection in trait $i$. This is because genetic correlations can arise among traits, either by linkage (close proximity in the DNA) or pleiotropy (when one gene affects more than one trait). For example, we may see no response at all in $i$ ($\Delta z_i = 0$) when both $G_i$ and $\beta_i$ are non-zero, if selection on a second unmeasured trait, $j$, opposes selection on $i$ ($\beta_i = -\beta_j$), and trait $j$ has equal variance ($G_i = G_j$) and is perfectly covarying with $i$, $cov_{i,j} 1$. Approximately this would be;

$\Delta z_i = (G_i \times \beta_i) +  (G_{i,j} \times \beta_j$)

$\Delta z_i = (0.5 \times 0.8) + (0.5 \times -0.8) = 0$

This is a major issue in the study of evolutionary biology. Genetic correlations can cause severe disparity between the actual and predicted response to selection and univariate methods are insufficient as a result. More studies adopt multivariate methods these days, though these are generally limited to just a handful of traits so its still not perfect. In reality methodological and logistical constraints present a huge obstacle to being able to predict $\Delta z_i$.


What is the name of this plant with mango type leaves?

This looks very much like a plant in the Ericaceae family, and specifically it looks to be some species of rhododendron.

Shrubby looking tree/shrub
Spirally arranged stiff (appears evergreen) leaves
Strong midrib on leaf
Large flower

With over 1000 species worldwide and more than 120 species known to occur in India, the picture likely doesn't have enough detail for someone without specific knowledge of Indian plant species to be able to ID to species. Even an expert might need the following details:

Exact leaf measurements, specific habitat details (elevation, distance to water, etc.) and closeups of leaf undersides, stem axils, bark and (opened) flower. A zoomed out picture showing the whole shrub/tree would also likely be helpful in IDing to species.

I would recommend reading Mao (2010) The genus Rhododendron in north-east India.

List of species and locations etc.

 Disclaimer: I am not very familiar with Indian flora, so I could be unaware of genera/species that might be a better fit. Please try using a flora with dichotomous key to ID.


Is there a theoretical maximum on the number of sexes a given species can have?

Well, your question as a whole is quite broad, with a lot of sub-questions or items (and some inaccuracies, as in the case of flatworms) . That being said, in this answer I'll address only your main question (and nothing more), which is ipsis litteris:

  Is there a theoretical maximum on the number of sexes a given species of organism can have?

All the content in this answer is based on this excellent book from Michael Majerus, Sex Wars: Genes, Bacteria, and Biased Sex Ratios:

Unfortunately, I don't have my library anymore and I can't find this book online. So, instead of (boringly) quoting the author, I'll try to summarise his hypothesis. Of course, to a better explanation, you can read the book itself.

Let's start supposing that you're pretty comfortable with the concept of sexual reproduction and sexual types, which I think you are.

Suppose we have two sexual types, called A and B. They have receptors in their gametes' membranes, in such a way that you cannot fusion A + A or B + B gametes, but you can fusion A + B gametes. If the A gamete could fertilize another A gamete, you'll have all gametes in a given gonad fertilising each other, which makes no sense. So, will assume that a given sexual type has mechanisms to avoid fertilising the same sexual type.

So far, what I described is the common system with two sexes, be them "+ and -" or "male and female", it doesn't matter.

Now, let's suppose three sexual types: A, B and C. For this to work, their membrane receptors must be such that A can recognise B and C, but not A. This is theoretically possible (although it is a mess genetically speaking). Thus, the possible matings are:

Sexual type A → A + B and A + C;
Sexual type B → B + C and B + A;
Sexual type C → C + A and C + B;

A system with 3 or more sexes has obvious advantages. Right now, for instance, in a population with two sexual types and the same sex ratio, one has 50% (1/2) of the individuals in that population as potential mate. But, supposing a sex system with 5 sex types (A, B, C, D and E), any individual would have 80% (4/5) of the individuals in that population as potential mate.

So, why cannot we find sexual systems with more than two sex types?

The answer is: we can, but not among species which perform fertilization (animals, plants, most of fungi, most of algae etc...).

This is the problem: in fertilization, or syngamy, the gametes don't simply join their nuclei. It's more complex than that: there is cytoplasmic inheritance, or extranuclear inheritance.

To keep the example among animals, the group you said you know best: mitochondria in the zygote comes from only one gamete (the female one). That happens to avoid what we call heteroplasmy, which is the presence of more than one type of organellar (mitochondrial, in this case) genome in the zygote.

In sex systems with only two sexual types the rule is very clear: "mitochondria comes from this one, but not from that one". That's it, case solved.

But what happens with our system with three (A, B and C) sexual types? If you define that when A mates with B only A donates the mitochondria and, similarly, if you define that when A mates with C only A donates the mitochondria, who donates the mitochondria when C mates with B? Do you see? There is no possible rule here!

Therefore, cytoplasmic inheritance is, probably, what avoids the evolution of more than 2 sexual types.

How can we support this claim?

Let's find what happens in species that perform sexual reproduction, but no fertilization (and, therefore, don't have the cytoplasmic inheritance problem). The best example are protozoans that perform conjugation.

Tetrahymena is a well known example. In these protozoans, according to Umen, 2013:

  An individual Tetrahymena cell expresses one of seven possible mating types (I–VII) that it faithfully and indefinitely maintains during vegetative propagation. After mating each new exconjugant has a recombinant micronucleus formed from its two parents. However, rather than just expressing one of two parental mating types, the sexual progeny of Tetrahymena undergo a kind of genetic roulette that allows them to choose at random up to seven possible mating types. (emphasis mine)

So, we have sex mating types. How that system works? According to Cervantes et al., 2015:

  The unicellular eukaryote Tetrahymena thermophila has seven mating types. Cells can mate only when they recognize cells of a different mating type as non-self.

Thus, if you belong to sexual type I you can mate with someone that belongs to sexual types II, III, IV, V, VI or VII. The same way, if you belong to sexual type II, you can mate with someone that belongs to sexual types I, III, IV, V, VI or VII, and so on...

The record, however, probably belongs to the basidiomycete Schizophyllum commune, with more than 28.000 sexual types! (Whitfield, 2004) To support the idea that cytoplasmic inheritance is in fact the main factor that avoids more than 2 sexual types, it's worth noting that biparental mitochondrial transmission is quite common in fungi (Barr, Neiman and Taylor, 2005).

Sources:

Majerus, M. (2003). Sex wars. 1st ed. Princeton: Princeton university press.
Umen, J. (2013). Genetics: Swinging Ciliates’ Seven Sexes. Current Biology, 23(11), pp.R475-R477.
Cervantes, M., Hamilton, E., Xiong, J., Lawson, M., Yuan, D., Hadjithomas, M., Miao, W. and Orias, E. (2015). Correction: Selecting One of Several Mating Types through Gene Segment Joining and Deletion in Tetrahymena thermophila. PLOS Biology, 13(10), p.e1002284.
Whitfield, J. (2004). Everything You Always Wanted to Know about Sexes. PLoS Biology, 2(6), p.e183
Barr, C., Neiman, M. and Taylor, D. (2005). Inheritance and recombination of mitochondrial genomes in plants, fungi and animals. New Phytologist, 168(1), pp.39-50.


Male-Male competition limited to breeding season?

It's strongest in the breeding season but male-male competition exists outside of the breeding season too, e.g. European Robins only breed in the summer, yet maintain territories year-round. It's pretty circumstantial, however sexual competition will only exist in the breeding season.

To address the Red Deer example, the deer only compete with antlers in the breeding season, but outside of the breeding season they aggregate in same-sex groups too, so most of the competition males will experience is male-male.

Normal behaviour will depend again on the species. Most birds I can think of have discrete breeding seasons and behaviour outside of this is rarely dependent on sex, generally including foraging etc. However I can think of many examples to this, such as Capercaillie, where the hens sometimes forage together. I suppose that 'normal' behaviour could be defined as any behaviour that is not part of the organism's motivation to reproduce.


Problem: What is this pattern of inheritance?

The answer is incomplete dominance.

It can't be codominance, because codiminance involves both phenotypes being expressed in different parts of the organism: you would end up with red and yellow spotted flowers.

It obviously isn't complete dominance, because the red x yellow cross produces orange flowers.

Knowing that it has to be incomplete dominance or multiple alleles, we can examine what we would expect to see in either of these cases.

Multiple alleles

In the case of multiple alleles, each individual plant has two alleles out of a possible three. These alleles will also express some sort of dominance pattern over each other. Let's say, hypothetically, that the dominance pattern goes Red > Orange > Yellow.

In this case, all of the yellow flowers would have a genotype of yellow/yellow. The orange flowers could be orange/yellow or orange/orange. Red flowers can be red/orange, red/yellow, or red/red. When performing the crosses between red and yellow, you would then expect some mixture of offspring, probably mostly red. If the dominance pattern was different, you would still expect to see some mixture of offspring. But instead we see only orange offspring.

Incomplete dominance

In this scenario, homozygote red individuals have a red phenotype, homozygote yellow individuals have a yellow phenotype, and heterozygous individuals have the mixed orange phenotype.

In this scenario, you would expect red x red to produce only red offspring, and the same goes for yellow x yellow, because both parents have to be homozygous. Orange x orange would produce offspring in a genotype ratio of 1:2:1, as is the case when you self-cross heterozygous organisms. Orange x red and orange x yellow will produce offspring in a 1:1 genotype ratio, as is the case when you cross a heterozygote with a homozygote. These are exactly the patterns we see, so we can conclude that the answer is incomplete dominance.


Yes, use the log-transformed phenotype. if you want to use a normally distributed error term, and this will only occur if the phenotype is log-transformed, then you must log-transform the phenotype.

The phenotype should be distributed in the same manner as the error term in your regression model of the GWAS.

$pheno = \beta_1 X_D + \beta_2 X_A +\epsilon$

$\epsilon = \mathcal{N}(x | \mu,\sigma)$

Following the central limit theorem, most of phenotypes are normally distributed.  However, there are cases where a Bernoulli distribution is correct, and a logistic style regression should be used.


Why aren't we allowed to refreeze previously thawed breastmilk in refrigerator?

This is just a guess, but I don't think this is a food safety issues, its more a case of 'this food is gross now' issue.

When I was a teenager I worked in a frozen food processing plant.  The freezers were giant boxes where freon was condensed on gigantic coils into a liquid and then the liquid freon would rain down on to the food passing under on a conveyer belt.  The vegetables were frozen instantly and it was quite tasty - frozen just a few minutes after being cleaned.

As industrial freezing is very quick and such flash freezing, the quality of the food is preserved in a pretty fresh state. [its horrible for the ozone in the atmosphere but this was in the 80s and I hope they changed the process].

Milk is a mixture of water based nutrients and globs of fat, which give the milk is homogeneous white color and its smooth texture.  Freezing milk in a typical refrigerator would take hours and ice crystals would form and separate out the two phases - the fatty portions would separate.  Try it with a glass of milk and see.   This is the same reason that you don't re-freeze ice cream, which has even heavier creme proportions (even fattier).  The texture is completely gone.


Is phosphofrucrokinase1 PFK1 found in the liver?

PFK2 (PFKFB2) doesn't appear to be present in the liver. The two sources I have used agree that PFK1 (PFKL) is present in the liver. They diverge regarding the levels of expression of PFKL.

This is the expression of the three 6-phosphofructo-1-kinase and one 6-phosphofructo-1-kinase genes according to the Human proteome map (mass spectrometry).

I can't see a huge dynamic range across the proteins in the liver, although the liver specfic gene (PFKL) is the 'winner' there.

The Human protein atlas (immunohistochemistry) is also a useful source for information and it provides a very different answer. Using immunohistochemistry it shows robust signal for PFKL but not for PFKFB2 in the liver.


How can binaural beats change mental state?

It is thought that binaural beats entrain the brain in the frequency of the binaural beat. These beat frequencies show up in the EEG.

The EEG in turn represents synchronous activity in the cerebral cortex (Fig. 1).

Fig. 1. EEG frequency bands and their associate mental states. source: Conor Russomanno

Now if you look at where 10 Hz EEG waves show up it is in the alpha frequency band associated with a relaxed mental state. The 40 Hz band on the other hand is associated with beta activity associated with an alert state.

Indeed, presentation of beta-frequency binaural beats have shown to improve the performance on psychophysical tasks and performances were better than when binaural beats were presented in the theta-delta range (Lane et al., 1998).

Reference
- Lane et al., Physiol Behav (1998); 63(2): 249–52


Why is nitrogen isotopic labelling required for protein NMR?

It is not strictly required. Isotope labelling is required when the usual isotope does not have a magnetic spin (for example 12C). 14N has a spin of 1 and exhibits 3 spin states: -1, 0 and 1. The isotope, 15N has a 1/2 spin. As noted in this book, analytical methods exist for both nitrogen isotopes.

However, 15N is preferred for NMR studies because the chemical shifts produced by 14N can be too broad to be detected by high resolution NMR spectrometer.

From wikipedia:

  Nitrogen-15 is frequently used in nuclear magnetic resonance spectroscopy (NMR), because unlike the more abundant nitrogen-14, that has an integer nuclear spin and thus a quadrupole moment, 15N has a fractional nuclear spin of one-half, which offers advantages for NMR like narrower line width.

From http://chem.ch.huji.ac.il/nmr/techniques/1d/row2/n.html:

  The 1D 14Nitrogen NMR experiment is much less sensitive than Proton (1H) but has a much larger chemical shift range. Its signals are broadened by quadrupolar interactions. The larger the molecule and the more asymmetric the nitrogen's environment, the broader the signal. Hence, the small and highly symmetric aqueous ammonium ion gives a very sharp line (fig. 3), less than one Hertz wide. Liquid ammonia, being less symmetric, is 16 Hz wide (on a 400 MHz spectrometer at room temperature). Urea is larger and asymmetric so the line-width is approximately 1 KHz. Molecules that are significantly larger than urea yield signals too broad to be observed with a high-resolution NMR spectrometer. However, the nitrogen chemical shift range is wide and so may be readily used for distinguishing nitrogen species for very small molecules.


What is the difference between copy number changes with and without allelic imbalance?

Allelic imbalance is a pretty broad phenomenon difference in the expression of two alleles.  As such you have listed would probably cause allelic imbalance, but it could be the result of methylation or even differences in RNA sequences between the alleles which say interfere with post translational splicing say.

In the case of copy number variations, if a copy number region (which is often a higly repetitive sequence in the genome and not a gene duplication) might interfere or not interfere with gene regulation. In cancer cells large segments of the genome may be copied or cut out though, so in that case the mechanism you put forth may be important.


Does xylitol kill all kinds of bacteria?

Xylitol does not kill any bacteria.

Xylitol is a sugar alcohol that bacteria happen to not be able to use as an energy source. In the absence of other sugars, bacterial growth slows. Therefore, its antimicrobial mechanism is bacteriostatic rather than bactericidal.

No antibiotic exists, or will ever exist, that kills or inhibits all kinds of bacteria.

One thing xylitol can kill is a dog – keep xylitol-containing products such as gum well out of their reach.


Task-dependent "reversed" handedness: why use left hand for some tasks? How is it controlled by the brain?

The dynamic-dominance hypothesis of handedness states that the essential factor that distinguishes dominant from nondominant arm performance is the facility governing the control of limb dynamics. Sainburg (1) writes that

  It should be noted that dominant arm advantages do not apply to all
  tasks, or all aspects of tasks. Healey et al. (1986) examined an
  extensive range of tasks and found that four factors or groups of
  tasks accounted for 80% of the variance in hand preference among the
  110 subjects tested. Tasks that were almost exclusively associated
  with dominant arm use included activities requiring precision in
  interjoint coordination and trajectory formation. (...) In contrast,
  tasks that involved spatially orienting a body segment posture were
  more often performed with the nondominant arm. These tasks included
  posturing the hand to point toward a distant object, which is similar
  to other functional tasks such as holding a piece of paper that is
  being cut with scissors, or orienting the hand in space for catching a
  baseball. Such postural orientation tasks are less dependent on
  intersegmental dynamics, since the trajectory used to attain the
  posture is not critical for task success. The dynamic dominance
  hypothesis thus appears to account for the extent to which hand
  preferences for specific activities are lateralized.

This appears to be consistent with your experience.


Dementia with Lewy bodies (DLB): It is characterized anatomically by the presence of Lewy bodies, clumps of alpha-synuclein and
  ubiquitin protein in neurons, detectable in post-mortem brain
  histology.[1] Lewy Body dementia affects 1.3 million individuals in
  the United States alone.

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

  Binswanger disease is a form of small vessel vascular dementia caused by damage to the white brain matter.[1] White matter atrophy
  can be caused by many circumstances including chronic hypertension as
  well as old age.[2] This disease is characterized by loss of memory
  and intellectual function and by changes in mood. These changes
  encompass what are known as executive functions of the brain.[3] It
  usually presents between 54 and 66 years of age, and the first
  symptoms are usually mental deterioration or stroke.[4]

http://en.wikipedia.org/wiki/Binswanger%27s_disease

To name the two with the highest prevalence after Alzheimer's and Parkinson's.


In our eyes, the dioptric difference between the dispersion of red versus blue light is approximately 2D.

Remembering that the human eye's peak spectral sensitivity lies at 550 nm (green), the human retina is deliberately placed such that it is in between the dispersion of white light, i.e., between red and blue. This optimizes the best level of focus specifically for its peak spectral sensitivity. The pupil and the nucleus of the lens also help to minimize chromatic aberration.

In short, the eye is constructed such that it is easiest to focus on green light, which is in the middle of the visible spectrum and has the strongest receptors.


Arm at Heart Level when Measuring Blood Pressure

This page (and many others) explain the idea rather well. This is more of a physics than a biology question, but the fundamental concepts are the same.

In fact, contrary to what you wrote in the question, the measured blood pressure should be lower than expected if the arm is elevated above heart level.

When you reduce the pressure on the bent pipe, the water level on the side where the pressure is reduced rises.

Similarly, When the arm is elevated, it is equivalent to the right hand side of the image, where the right hand tube's water level is higher than the left hand side. Raising the arm above heart level, with the pressure of blood at the heart level remaining constant, will result in a lower pressure being measured, due to the heart effectively having to pump the blood up the distance.

For the same reason, giraffes have very high blood pressures (double that of humans) due to their long necks. If their blood pressure was at the level of humans, they would faint when raising their necks, due to the blood pressure falling to zero at their brains.


According to Clinical Neurophysiology of the Vestibular System
 By Robert William Baloh, Vicente Honrubia, page 8, the vestibular system (animals' "accelerometer") is as old as 600 million years and is present in invertebrates.

I assume (without a precise source) that this is especially important for flying insects (after all, accelerometers were engineered for flying machines in the first place!) and that the ant didn't respond because the acceleration to which you submitted it was not deemed harmful.


In CRISPR bacteria, how does viral genomes get integrated into the spacers of CRISPR? Also, in its use, where does Cas9 cut the DNA?

This paper should clear up a lot more than anyone on here truly can about the CRISPR system.

CRISPR/Cas9 is very unique, even compared to other proteins purified from bacteria like Taq Poly.

The reason is due to how complex it is actually induce this protein. Essentially you are transfecting a plasmid with the Cas9 protein and its guide RNA (gRNA) on the vector. Transfecting itself is not easy, not to mention you are essentially adding a mechanism to a cell trying to knockout genes and you've got a handful. In fact doing that for one cell line, and noting the effects of what you knocked out, would be enough to produce a paper in a pretty impactful journal. (Image from: https://www.systembio.com/)

Also some recent advancements in CRISPR include:

Light-induced CRIPSR/Cas9 (easier regulation of enzymatic activity)

Basically these researchers were trying to deduce a method allowing for more control of the CRISPR technique, since CRISPR has had issues with off-target effects. While it isn't a change in how CRISPR works, or even where, the change is how much you can control the reaction. Simply put they devised a way that allows you to turn CRISPR on/off using light allowing more precise control of its activity. Surely it will be helpful to reduce off target effects.

"This was accomplished by fusing the light-inducible heterodimerizing proteins CRY2 and CIB1 to a transactivation domain and the catalytically inactive dCas9, respectively." (Lauren R Polstein & Charles A Gersbach)

Cpf1 to replace Cas9 as cutting protein (more percise activity)

This one is a bit more interesting in that it is a direct change to the CRISPR system itself. Cas9 has been the standard cutting protein used for the CRISPR system although it has had controversy due to its somewhat imprecise cutting. Cpf1 has been shown to be more precise (so their data says) and it is now being implemented by some to see if this is truly the case. Combined with the above "light-induced" system this brings CRISPR down to safer levels when talking about off-target effects.

Here are some good online seminars to get you started:

CRISPR/Cas9 from start to finish
Improve CRISPR-Cas9 experiments with rationally designed guide RNAs

These seminars I can't really comment directly on because they explain everything so well on their own. Anything I say really will only detract from what they are teaching since I am by no means an expert with CRISPR but simply someone who is looking into possibly using it for my lab. Right now there is a lot of guide material on how to properly format your CRISPR experiments but my personal opinion is to give the technique maybe a year or two more when it is more standard for research.

That is unless you want to directly research the method and improve it in your own way.

Let me know if this answers your questions sufficiently.

Sorry that I cannot do much more in terms of explaining the links. The studies are not ones I can easily access unless I am at work since I usually access them through the university.

As far as the repair mechanism goes (your #3 question) I can't really answer that for sure but I have recently received a pamphlet that describes how to ensure the cells uses HJ rather than NHEJ.


Generally textbooks take the following pedagogical flow in basic neurophysiology:
Ions flow, so voltage changes propagate
This is the "electrotonic part". The key concept is that if you add some ions or change the voltage of one part of a neuron, adjacent areas will also change in voltage as current flows 'passively'. The further away you go, the longer it takes the signal to arrive and the smaller it will be as the charge spreads out.
A more advanced course might also talk about the sources of those charges, like sensory receptors or neurotransmitter action, and might talk about the ways that polarizing pulses integrate over space and time. Or these may be saved for later.
(side note: in reality, neurons aren't all that passive, there are lots of conductance changes occurring even in this supposedly "electrotonic" scheme, but the electrotonic equations tend to work pretty well, and in a simplified experimental system they are sufficient. Biology is almost always too complex to try to include everything at once)
Action potentials
The key concepts here are that if the voltage changes enough, it stops being possible to think about just the passive flow, you now have to think closely about voltage-gated channels that create a positive feedback loop response to voltage. Above threshold, voltage-gated channels cause sufficient depolarization that adjacent areas of the membrane are also depolarized beyond threshold, and we call this propagating signal an action potential.
At this point, you are supposed to remember and understand that what is driving this active response is still a somewhat "passive" flow of charge that you understood from the "electrotonic" part of the course. That part is the physics and is always present, you can't get rid of it. However, you're in a new scheme where you can't use the electrotonic equations to understand what happens anymore.
Saltatory conduction
Myelination and saltatory conduction comes next. In this section, you're supposed to be thinking about the way action potentials spread, but to add one extra little wrinkle. What if, instead of transmitting piecemeal to the next adjacent segment of membrane, axons were more insulated? In this scenario, the flow of charges will extend much further. You should still be applying the concepts you learned in the "electrotonic" part, though: if you add some ions/change the voltage of one part of the neuron, adjacent areas will also change in voltage as current flows. The further away you go, the longer it takes the signal to arrive and the smaller it will be as the charge spreads out.
Therefore, even though insulation lets the signal travel further, it still decreases in amplitude over long distance, and you need to "boost" the signal again. That's where nodes of Ranvier come in.
Back to your specific question...
"Does electrotonic spread/conduction occur in saltatory conduction?" - No, but not because the "physics" part is different: saltatory conduction is necessarily active (involves voltage-gated channels), not electrotonic, even though all the electrotonic principles still apply.
The "electrotonic" part of the lesson contains important concepts that you are supposed to remember and carry through the other sections, even if it's not discussed explicitly. I think making that active/passive distinction is possibly a bit misleading, but the concepts you are supposed to grab from the electrotonic section in terms of the physics of how charge/voltage moves around in a neuron applies to everything.
Additionally, you should gather that the nodes of Ranvier are spaced in order to conduct action potentials. These are big voltage changes. Smaller voltage changes that are subthreshold will of course also travel down the axon (this is the physics part - nothing stops physics!), but if they aren't strong enough to open voltage gated channels at the next node of Ranvier then the voltage change isn't of any consequence and just decays with distance. If it was strong enough, then by definition it is superthreshold rather than subthreshold, and we are talking about an action potential.

All the content in this answer is material like you would find in a basic undergraduate neuroscience textbook. The ones I usually recommend are Purves or Kandel.


Evolutionary answer: I like to go one step before green plants and consider the humble alga. Algae were historically classified as green, red, and brown, based on the wavelengths that their characteristic pigments absorbed. It is believed that land plants evolved from a common ancestor of algae, so you might wonder why we don't have similar broad categories of green, red, and brown plants.

Our best guess is that the organisms we call "plants" came from a single evolutionary event and share a common ancestor with green algae, rather than a different group. These green plant-like beings were probably the first big land organisms to try photosynthesis and happened to do well enough to out-compete any other plant-like being that might arise in their environment. Being green was "good enough" to for photosynthesis, allowing these organisms to survive and thrive.

Meta-answer: "Why" questions in biology often have probabilistic (and intuitively unsatisfying) answers. It's very hard to collect data that can "prove" why certain things evolved the way they did. Plus, evolution is not an engineering or design process. It leaves dead ends and doesn't always find the right solution. Founder effects can be very strong. But organisms which last long enough for us to study tend to be "good enough" at what they do. Here, the most parsimonious explanation for why leaves aren't black is that land plants came from green algae and didn't need to produce more of other pigments to take over the world.

Biochemical side-note: Plants can suffer from photooxidative stress when exposed to intense light due to the generation of reactive oxygen species, which disrupt metabolism. Therefore, some non-green pigments, like xanthophylls, are actually responsible for quenching chlorophyll and dissipating energy away from light-harvesting complexes. More energy is not always a good thing.


How does heart beat faster while doing a strenuous task?

I am sure that there are many ways that your body can regulate heart rate, but I am going to cover this topic briefly from the perspective of $\ce{CO2}$/$\ce{O2}$ concentrations, and pH.

The medulla oblongata

The medulla oblongata is part of the central nervous system, and makes up the lower portion of the brain stem. It is responsible for performing autonomic functions, including the regulation of heart rate through chemoreceptors. The medulla oblongata receives its blood supply from the vertebral artery and makes both afferent and efferent connections with the vagus nerve.

Chemoreceptors

There are two main types of chemoreceptors in your cells that are responsible for regulating heart rate.

Central chemoreceptors

These are located in the medulla oblongata, and are responsible for measuring the concentration of $\ce{H+}$ ions (ie. pH). When the pH is low, neural cells with these receptors will signal the release of norepinephrine and epinephrine.

Peripheral chemoreceptors

These are located in the carotid and aortic bodies and measure the concentration of $\ce{O2}$. The receptor cells of these structures make connection with afferent nerves, to send a signal to the central nervous system in times of hypoxemia.

$\ce{CO2}$/$\ce{O2}$ Exchange

Blood is the tissue responsible for distributing chemicals around your body. It is therefore also involved in the $\ce{CO2}$/$\ce{O2}$ exchange between tissues. Blood cells use hemoglobin as as a carrier molecule for this exchange.

When $\ce{O2}$ is delivered to tissues, it will be processed by the mitochondria of the cells to synthesise ATP, and $\ce{CO2}$ as a biproduct. ATP is also responsible for muscle contractions, and so, with exercise comes an increased utilisation of ATP. With ATP stores running low, your cells will begin to use more $\ce{O2}$, and therefore, they will produce more $\ce{CO2}$.

$\ce{CO2}$ and Acidity

So, I kinda lied when I said hemoglobin is the carrier of $\ce{CO2}$. This is mostly true, but $\ce{CO2}/$$\ce{O2}$ is also somewhat soluble in blood, and this accounts for changes in blood-pH.

$\ce{CO2 + H2O}$ $\ce{<=>}$ $\ce{H2CO3}$ $\ce{<=>}$ $\ce{HCO3- + H+}$

The above equilibrium is catalysed by carbonic anhydrase, and accounts for a decrease in pH levels.

Signalling in response to pH

So your exercising, your body is using lots of $\ce{O2}$ to produce ATP. Your $\ce{CO2}$ levels have increased, and your internal pH has dropped. Now what?

Well, as I'm sure you have guessed, your nervous system takes over.

The central chemoreceptors of the medulla oblongata send an impulse to  the adrenal glands in response to the decreased pH. This signals the release of the hormones epinephrine and norepinephrine in to the bloodstream. The release of epinephrine and norepinephrine is regulated by the sympathetic nervous system. This accelerates the heart rate by binding β-receptors in your heart tissue. Efferent nerve connections from the vagus nerve also participate in this process (I think).

For mechanisms on heart contration, see here; everything following "excitation contraction coupling" is probably the most relevant.


In men, why do over 80% of sperm have abnormal form?

So I've dug a bit into how a 'normal morphological' form is defined and characterised, since assessing morphology into 'normal' and 'not normal' is always a very tricky thing.

Looking into the method section of the source you cited, we get:

  All laboratories generating the data analysed here used standardized
  methods for semen analysis [...] The various editions of the manual provided similar
  methods for assessing sperm concentration, motility and morphology but
  provided different criteria for categorising morphology.

So the  problem begins already with the fact that there is not one, but multiple different recommended practices.
(For anyone interested the different staining methods used were: Bryan–Leishman [B], DiffQuik [D], Haematoxylin and Eosin [H], Papanicolaou [P], Quickdip [Q] and Shorr [S]. Of thses H, S and P were used for generation of the 'normal morphology' reference set).

Clearly this problem was also obvious to the authors, so they tried to restrict the data they used:

  Although all centres reported using WHO procedures, the recommended
  methodologies have changed over time, and many centres have
  experienced difficulties with the subjective assessments of
  morphology. Data on normal sperm morphology were only included if
  results were reported as determined according to the so-called
  ‘strict’ (Tygerberg) method (WHO, 1992, 1999).

Fortunately these WHO guidelines are available on Google Books and they require the following points to met (most of which were defined by 95% confidence intervals of control samples):

head length 4.0-5.0µm
head width 2.5-3.5µm
head length-to-width ratio 1.5-1.75
well defined microsomal region compromising 40-70% of the head area
mid piece should be slender, <1µm
[mid piece should be] 1.5x size of the head
[mid piece should be] axially attached to the head
Cytoplasmic droplets should be less than half size of the head
Tail should be [...] approximately 45µm long

Plus one very important sentence:

  This classification scheme requires that all 'borderline' forms be considered abnormal

This sentence is important, because it means that each criterion stated has to be fulfilled for a single sperm to classified as morphological normal.
If we take only the numeric requirements (which should cover ~95% of the normal value distribution for a healthy population) and assume that they are not correlated, this means that for any given single healthy sperm we have a $0.95^9 = 0.63 = 63\%$ chance that it is within the 95% interval of all defined parameters.
This means that applying this strict categorisation scheme should even for a 100% healthy population only result around 63% sperm cells categorised as morphologically normal (ignoring that the parameters are probably not interdependent which would make it a bit better).

If we now take into account that the analysed samples were probably not 100% healthy cells and remember that the (reported) difficulties of assessing morphology, I think that the reported values for 'morphological normal' are not as quite as unexpected as they might seem.

Note: all bold highlighting in the quote blocks was added by me.


What is the difference between osmotic potential and osmotic pressure?

Osmotic pressure: pressure applied by a solution to prevent the inward flow of water across a semi-permeable membrane.

Osmotic potential: the potential of water molecules to move from a hypotonic solution to a hypertonic solution across a semi-permeable membrane.

Osmotic pressure can be calculated using the following formula:

$$Π = iMRT$$

where
$Π$ is the osmotic pressure in atm

$i$ = van 't Hoff factor of the solute.

$M$ = molar concentration in mol/L

$R$ = universal gas constant = 0.08206 L·atm/mol·K

$T$ = absolute temperature in K

The following page has a worked out example.

As for your question on solute potential vs osmotic potential, the answer is that they are indeed the same. You can compare the formula for $\Psi_{\pi}$ on the wikipedia page and the page of this pearson textbook. These formulas are the same:

$\Psi_{\pi} = -Π =-iMRT$

So there's a simple relationship between osmotic pressure and osmotic potential.


Do proteins generally contain phosphorus and sulfur?

Of the 22 known proteinogenic amino acids, all contain hydrogen, carbon, nitrogen and oxygen. Some (methionine and cysteine) contain sulfur while one (selenocysteine) contains selenium. None contain phosphorus, but this element can be incorporated by:

Post translational phosphorylation of various residues. This often allows/prevents binding of other proteins and/or triggers a conformational change in the target protein. It is also necessary for proper folding of some proteins (example). Sulfur can also be incorporated in a similar manner (sulfation).

Incorporation of phosphorus containing prosthetic groups. This can occur covalently and is necessary for the function of some proteins. Sulfur can also be incorporated as part of prosthetic groups.

You may also consider the other elements necessary for the structure/function of many proteins: iodine in thyroglobulin, iron in hemoglobin, etc...


An uncom-petitive inhibitor doesn't compete with the natural substrate of the enzyme for active site i.e. it binds at a site distinct
from the substrate active site and binds to the $ES$ complex.

$K_I$ is the equilibrium constant for inhibitor binding to $E$ and $K_I^{'}$ is the equilibrium con-
stant for inhibitor binding to $ES$. Uncompetetive inhibitor lowers the value of $V_{max}$ and $K_m$.


All of these are affected by specific characteristics of the nociceptors.

Nociceptors are only sensitive to high pressure. The low pressure stimulus would only stimulate mechanoresceptors which would not cause a perception of pain. Receptors like $TRPA1$ sense mechanical stimulus of a higher degree. $P2X/P2Y$ sense ATP which is released due to mechanical tissue injury, as mediated by high pressure or a sharp object injury. Further more, several cells die as a result of nociceptive mechanical stimuli releasing mediators the receptors to which also act as nociceptors.
Exaggerated response to a noxious stimuli is called Hyperalgesia. A sensation of pain in response to a normal stimulus is called Allodynia. Both of these are mediated by specific sensitizing receptors on the nerve endings sensitive to Bradykinin, %HT, Serotonin, Substance P etc. All these are commonly found in conditions where these two are observed, as in the case of burning on touching following sunburns, or increased pain adjacent to an inflammatory foci.

Source:- Ganong's Review of Medical Physiology


Because your teeth evolved as a sensory organ.
The material teeth are made of evolved first in placoderms, it existed to sense the electrical current in the water around it, so it has to form around a nerve. in modern animals the nerve mostly functions in sensing stress and thermal stress on the tooth.
And because mammals are weird.
Teeth did not evolve to be permanent, they evolved to be lost and replaced, that is what everything that is not a mammal does. So having a nerve was not a big disadvantage (in say, reptiles) since that nerve would eventually wither and die as the tooth was lost. toothaches were not permanent they were a temporary irritation, and served do dissuade any behavior that caused them, like trying to eat food that was too hard, it was little different than the pain of thorn telling you not to grab sharp things.
Mammals are unique in retaining their teeth throughout their life so now a system shaped by evolution to be temporarily has been dragooned into something permanent. So now what would be a temporary irritation becomes a permanent thing when the tooth is damaged in mammals. Worse permanent teeth means things like stress on the teeth is even more important since you are stuck with damaged teeth so mammals actually make the nerves bigger. The addition risk of a toothache is not an issue because mammals are stuck with that risk anyway because they retain the tooth. The earliest mammals did not have long lifespan so the risk of a debilitating toothache was minimal, however we their descendants live for decades, so a structure evolved to last a year or two now has to survive for decades and it just fails sometimes. Evolution can only change what it has it cannot throw out a problematic system and start over from scratch, so it often gets stuck with such haphard thrown together solutions (kluges) And we unfortunately have to pay the price in this case


What are the difficulties/challenges against developing a coronavirus vaccine?

There are multiple challenges presented, and many of those are not limited to coronavirus vaccine.

As mentioned above, it just takes time. Before a vaccine can be used in patients, clinical trials must be performed to validate the safety and efficiency of the vaccine candidate. A Clinical trial includes three phases, which again, just takes time.

But to really answer your question, what are some challenges of developing a vaccine?

To begin with, from the perspective of lab research, we first need to develop a vaccine candidate. What protein on the virus should we take as an antigen? There are many many proteins on the virus, and for CoV, we know it is a protein called Spike protein. It is the neutralizing target on the virus. Which means, when an antibody bound to this site, it could prevent the virus from infecting the cells. Okay, then we have to know, do we need to do something to this protein to make a vaccine? For example, when we try to manufacture this protein into a vaccine, what if the protein is degraded? Or it somehow becomes a 'bad' protein that simply cannot stimulate immune responses in human? These are just some examples of roadblocks of developing vaccine.

Let's suppose we finally work those out. Then what's next? Each candidate vaccine needs to be tested in animals before going into human clinical trial. This step is time-consuming.

Now we are finally ready to start clinical trials. According to FDA, the vaccine for human trials (also for each drug) needs to be produced under Good Manufacturing Practices (GMP). It's basically a standard operating procedure to make sure that the vaccine candidate can be manufactured in a large-scale, quality-controlled manner. There are many many challenges, like how to purify the protein? How to scale-up production. This is partly of the reason why the first vaccine in trial in USA is an mRNA, and in China is a DNA, both of which does not require complicated protein purification.

As you can see, the list of challenges can go on and on. But there are scientists and doctors working diligently on it. Hopefully we'll get there.


What species is this aromatic plant found in a mountainous region of Greece?

A type of greek lavender with no blossoms anymore?
https://www.florealpes.com/photos/lavandulastoechias_5.jpg?PHPSESSID=0a72039f5036d91c7df80dd406b795b0


Why don't cells of aquatic animals burst?

Comparative physiology of body fluid regulation in vertebrates

Cells are not passive components that always return to osmotic equilibrium. Through hormonal, cell signaling, and the number of pores for ion and water exchange marine animals can maintain osmoregulation in various aquatic environments. In land mammals osmoregulation is more passive since it is controlled by the endocrine system.


Why do flies "rub" their front legs when resting?

Flies rubbing their legs are cleaning themselves. They can also often be seen rubbing their back legs often. Additionally, flies also often clean their wings, compound eyes and bodily bristles. Legs and wings are used as a primary means of locomotion and means of escape. Eyes and bristles are sensory organs and hence also essential for their survival.

Below a picture of a tachinid fly showing the bristles and compound eyes:

The eyes need to be clean as they are essential for the detection of visual stimuli. The bristles, as a commenter rightfully stated, contain chemoreceptors reminiscent of receptors on the human tongue that sense sweet and bitter tastes. These taste receptors alert the fly for sweet (food) and bitter (poisons) substances. Hence, cleaning of the legs may not only serve hygienic purposes, but may well be important for keeping the bristles and hence the associated sensory organs clean and free of prior encountered substances.


Why are sequencing reads shorter than PCR products?

Reliable sequencing reads start usually 50bp downstream from start of primers. Which means that 180bp-band (on the gel) sequenced with one primer will yield readable sequence in region 50-180bp (130bp length). Also I notice that sequences usually reported somewhat before reliable data, i.e. clean data starts after 52-55bp, but sequencing reports basepairs downstream from 48bp after primer start.

If you need whole-band sequence, you will have to sequence with set of two primers, each in different direction. Since you PCR this band, you already have your sequencing primers.


Without going into Down syndrome specifically, let's address the title of your question: Why is trisomy a problem? Or, more specifically, why can it be a problem to have extra copies of genes?

Let's imagine biology to be just a really complicated cake. If you are trying to bake a cake, and you leave out the flour, I think mostly everyone would agree that the outcome product wouldn't be much of a cake at all: that's the condition where you are completely lacking an ingredient, both copies of the same chromosome, a nearly assured fatality.

But let's say you instead include 50% too much flour. What results? You might still get a cake, but it might not taste perfect: maybe a little too bread-like or not sweet enough.

In short: having an extra chromosome means genes on that chromosome are overexpressed. Those gene products could themselves have deleterious effects in excess, or they could affect expression of other genes and cause over- or under-production of those products. Of course it isn't as simple as "+50% expression!" because of regulatory mechanisms ubiquitous in biology, but there is sufficient overexpression to cause some issues.

Really, someone with Down syndrome develops almost completely normally - many other trisomys are fatal in the early stages of development, so we don't become familiar with them. For Down syndrome in particular, you can check out some of the proposed mechanisms on Wikipedia. One suggestion is that some of the cognitive deficits resemble Alzheimer's disease, implying a causative function for amyloid beta in both circumstances. The hypothesis is that amyloid beta accumulates in aging brains, but people with Down syndrome overproduce amyloid beta so they show dementia symptoms much earlier. This comparison is certainly not the only factor in Down syndrome, however.


How Do Large Ocean Viruses Form Their Own Organelles?

The organelle form in the same way they would if they were coded for by the host's genome, except in this case the virus uses its own genome to specify the type of organelle.

The article you link to indicates this.  The "systems" in the quote are in part the organelle that it needs

  A study of the giant virus’s DNA shows it to have over a thousand genes, the biochemical instructions it uses to build the systems it requires to replicate once inside its host.


Purpose of dilution streaking or streak purification

The purpose of this technique is to dilute the bacterial cells so much that you get single cells, as can be seen on the image of the plate. You can then pick the colonies grown from these single cells, characterize them, test them for the mutations/plasmids, or whatever change you introduced, and can be sure that you have only the descendants of a single cell in your culture.

This way you ensure that you don't grow a mixture of different cells with different characteristics, of which one will eventually overgrow the other one. The streaking is a fast and reliable technique, which works especially well when you want to test a larger number of bacterial cultures. It also allows to check a stock culture very fast for contaminations with other bacteria by simply inspecting the single colonies by eye (different bacteria often look different).

Diluting the cultures would work as well, but needs to be done in more than one step and is more work when you want to do it for more than one culture. Also for dilutions you often plate more than one plate to be sure to have a plate with single colonies (when the cell number is unknown).


What's the proton concentration around a DNA helix?

DNA stands for deoxyribonucleic acid. Acid, by definition and mechanism in aqueous environment, is something that donates proton ($H^+$). HCl dissolved in water will donate proton to solution, thus bringing pH down, since $pH=-log_{10}[H^+]$.

DNA, being an acid, donates protons to water and brings pH down a notch. Just like in case with HCl, it has nothing to do with keeping charge neutrality. Water is not a buffer, that is able to tolerate or smooth change in pH. What happens when you add DNA to buffered solution, say phosphate buffer, is completely different story from biochemistry.


Potassium channels participate in controlling the concentration gradient of the cell.

I would rephrase this to "Sodium/potassium pumps establish the concentration gradients of sodium and potassium across the cell membrane." Potassium channels do not.

  I have found evidence in articles supporting the first claim, but I
  don't know much about the second.

Right; because the channels don't set up concentration gradients.

  Do potassium channel blockers affect the resting membrane potential?

If they block the resting state "leak" potassium channels, you bet. The resting membrane potential is largely set by the electrical conductance through those channels. Blocking them would greatly depolarize the cell compared to typical resting membrane potential values. But there are many different potassium channels. You may be thinking of blocking the delayed rectifier potassium channel, which shouldn't do much at all to change the resting membrane potential.

  Would they significantly alter the concentration gradient?

Probably not, since though the cell would be losing less potassium through this conductance, what matters more to the concentration gradient of potassium are the sodium/potassium pumps.


Is it possible to genetically modify a plant at home?

Well, that depends on your home. ;) I think it is not an easy process.

There are two main methods that are used to genetically modify plants:

Using the bacterium, Agrobacterium tumifaciens, as a vector for the DNA. Agrobacterium has the ability to infect plants and insert DNA into a plant's genome. It causes crown gall tumours in natural infections. This method has mainly been used to modify broad leaved plants, such as sugar beet and oilseed rape, but is now also being applied to monocot species, such as maize and rice

Particle bombardment or biolistics where the DNA to be inserted is coated on minute gold particles and fired into plants cells. This approach is used for monocot plants such as maize and rice

Here I found simple step by step article, but lil bit old. may be there are new methods for this process.
How To Genetically Modify a Seed, Step By Step


Hemoglobin molecules used to manufacture these products are not
  contained by a red cell membrane, and when released into the
  vasculature, these molecules rapidly scavenge nitric oxide.This can
  result in systemic vasoconstriction, decreased blood flow, increased
  release of proinflammatory mediators and potent vasoconstrictors, and
  a loss of platelet inactivation,17- 20 creating conditions that may
  lead to vascular thrombosis of the heart or other organs. This
  mechanism has recently been shown in preclinical models to be
  responsible for injury during hemolytic states, in which hemoglobin is
  also released into the circulation.21

  Unlike naturally occurring hemoglobin, manufactured cell-free
  hemoglobin-based blood substitutes (HBBSs) can be chemically altered
  to theoretically minimize such toxicities. It has been postulated that
  cross-linking, polymerization, or pegylation of hemoglobin will create
  larger, more stable HBBS molecules, preventing extravasation and
  thereby leading to a reduction in toxicities related to nitric oxide
  scavenging. At least 1 manufacturer has also chemically increased the
  affinity of its HBBS for oxygen (lower P50, the partial pressure of
  oxygen required for 50% hemoglobin saturation) to decrease arteriole
  oxygen transfer and thereby potentially eliminate untoward
  cardiovascular effects.

2008 - Cell-Free Hemoglobin-Based Blood Substitutes and Risk of Myocardial Infarction and Death

So cell free hemoglobin is toxic. As you can see this toxicity can be reduced in other ways too, so it seems like there is an evolutionary pressure in the direction of having blood cells, maybe it is simpler this way. To answer the other question, I think there can be free HGB in the blood when blood cells fall apart because of an infection e.g. malaria, etc...

  Hemolysis in falciparum malaria results in NO quenching by cell-free
  hemoglobin, and may exacerbate endothelial dysfunction, adhesion
  receptor expression and impaired tissue perfusion. Treatments that
  increase NO bioavailability may have potential as adjunctive therapies
  in SM

2008 - Relationship of Cell-Free Hemoglobin to Impaired Endothelial Nitric Oxide Bioavailability and Perfusion in Severe Falciparum Malaria

Btw. I agree with rhill45, I think too that it is easier to regulate O2 and CO2 exchange if you have a specialized cell type, so it might have regulation purposes. It can have recycling purposes either, because it is hard to distinguish between old (damaged) and new HGB when they are in a cell-free form. This problem probably can be solved by destroying only glycosylated hemoglobin, but I guess it is much easier to filter out the old RBCs in the spleen...

  In the process of maturation, a basophilic pronormoblast is converted
  from a cell with a large nucleus and a volume of 900 fL to an
  enucleated disc with a volume of 95 fL. By the reticulocyte stage, the
  cell has extruded its nucleus, but is still capable of producing
  hemoglobin.

according to wikipedia (without citation).

Other sources claim the same, with the extension that this period lasts only for a short time, because the cell soon loses its mRNA and so it stops producing HGB. So according to these articles RBCs create the HGBs in the early stages of their life. (I did not find a real scientific article about this, but I can accept this theory.)

According to Chris this toxicity is just a protection mechanism, so I dug deeper.

  Bacterial virulence is greatly enhanced by freely available iron, such
  as that in fully-saturated transferrin or free haemoglobin. Following
  trauma a fall in tissue Eh and pH due to ischaemia, plus the reducing
  powers of bacteria, can make iron in transferrin freely available and
  abolish the bactericidal properties of tissue fluids with disastrous
  results for the host. Hyperbaric oxygen is a possible therapeutic
  measure that could restore normal bactericidal systems in infected
  tissues by raising the Eh and pH.

2006 - Iron and infection: the heart of the matter

  Iron lies at the center of a battle for nutritional resource between
  higher organisms and their microbial pathogens. The iron status of the
  human host affects the pathogenicity of numerous infections including
  malaria, HIV-1, and tuberculosis.

2012 - Hepcidin and the Iron-Infection Axis

So RBCs protect the iron against microbial pathogens, that's their key role. I think every other related problem, like O2 release regulation, free HGB toxicity, HGB recycling, etc... can be solved with free HGB as well, so most probably iron protection is the evolutionary pressure to store HGB in blood cells instead of letting it be in the blood in a cell free form. It's funny that every single book gets this wrong, and they claim that carrying oxygen is the most important role of this cell type, while they aren't mention anything about iron protection... :-)


Are there any animals that get smaller as a normal part of their life cycle?

In holometabolous insects it is quite common for the final larval stage to be heavier than the adult stage. For instance, Goliathus beetles, which are among the largest insects on earth, the adult stage often weighs about half of the final larval stage (which weigh 80-100 grams).

The same situation can be seen in the Hercules beetles, which this picture of both larvae and adult of Dynastes tityus clearly shows:

.
(picture from http://harrellhouse.com/in-the-museum-eastern-hercules-beetles/)


There is no water escaping from the coconut seed. The transformation of coconut water into coconut meat is explained by the development of the endosperm.

What happens is that, after the (double) fertilization, the endosperm of the coconut forms by nuclear division without cellular division, that is, without the formation of cell walls. This is called nuclear endosperm. According to the Wikipedia link above:

  Nuclear endosperm formation → where repeated free-nuclear divisions take place; if a cell wall is formed it will form after free-nuclear divisions. Commonly referred to as liquid endosperm. Coconut water is an example of this. (emphasis mine)

So, in an oversimplification, think about the coconut water as the cytoplasm of a single, huge cell, full of hundreds of nuclei.

After some time, cell walls surrounding the nuclei start to form. This is what we call cellular endosperm. According to the same link:

  Cellular endosperm formation → where a cell-wall formation is coincident with nuclear divisions. Coconut meat is cellular endosperm. (emphasis mine)

Therefore, in the coconut, the endosperm is initially nuclear (coconut water) and, after some time, becomes cellular (coconut meat).

According to Abraham and Mathew (1963):

  Cellular endosperm development becomes visible in nuts about 6 months old, at which stage a thin coating of jelly-like endosperm tissue is seen around the periphery of the large embryo-sac cavity.

This image shows those two tipes of endosperm (and helobial endosperm as well):

Source:

ABRAHAM, A. and MATHEW, P. (1963). Cytology of Coconut Endosperm. Annals of Botany, 27(3), pp.505-512.


This is quite common. It is most likely dried rheum (also know by slang terms such as "sleep", "eye boogers", "eye crusties", etc.).

Rheum is the result of dried mucus, tears (and the salt and minerals therein), as well as dead blood and skin cells.

Essentially it is all the stuff that’s normally in your eye that eventually dries up making the contents more condensed giving it a light yellow color. When all that stuff is in your tears it is spread out enough that your tears are still mostly clear.


What is the smallest scale at which blood vessels, nerves and other structures are deterministic?

Indeed a very good question. I'm afraid it might remain without a proper anatomy-based answer, but my intuition would tend towards agreeing with "the smaller you get, the more deviation you'll find".

Or rather, I would expect the same principle as in conservation of genetic patterns to apply here: the more central a tissue structure is to survival, i.e. the more downstream systems depend on it, the more likely it will grow in conserved patterns.

As an excellent example, the largest blood vessels including the aorta and its first- and second-degree branches are identical in branch number, approximate relative branch size and approximate branching location across probably all living humans (given that babies born with malformations on this scale would probably not survive without drastic surgery). Similarly, the largest-level nerves and nuclei are identical across the species. These are central systems that provide core functionality for survival.

On the other hand, teeth are quite important, but the odd tooth missing or additional doesn't harm terribly as no downstream systems depend on them. Indeed, it isn't uncommon for humans to be missing a permanent tooth and keep their primary (baby) tooth in that spot for decades; similarly, missing 8th teeth or additional 9th teeth also occur.


Are the byproducts of mammalian digestion simply depleted versions of the food or liquid consumed?

The answer really depends on what aspect of the urine and feces one is considering.

On the atomic level, no, urine and feces are composed entirely of atoms taken from our environment. As one would expect, as there is no "Humanium" on the periodic table. In fact, all the atoms in urine and feces were originally created by stars.

On the molecular level, yes. The body produces molecules that we do not ingest, or that we ingest in minute quantities, such as urea and bile.

On the cellular level, yes. The body produces, for instance, red blood cells even if the person eats a vegan diet with no blood intake. The proteins that make up the cells are created by breaking down ingested proteins into their constituent amino acids, which are then used to construct new proteins.

Also at the cellular level are the huge amount of bacterial cells that we support. Estimates of the number of bacterial cells in our body range from ten to 100 times the number of our own cells. The bacterial component in feces is massive - up to 1/3 of feces by weight are bacteria. Urine, being produced from the blood by the kidneys, is relatively sterile.


Reason behind formation of positive supercoils during DNA replication/ transcription

It's hard to explain in text, so here's a video:

https://www.youtube.com/watch?v=J4YlcD59-yw

Imagine the shoelaces are two DNA strands in a double helix. They are topologically constrained at each end. As the pen (helicase) moves through the helix, it creates overwound DNA in front of it and underwound DNA behind it.


The main families of calcium-gated channels I am aware of are the calcium-gated potassium channels and the internal ryanodine receptors involved in calcium-induced calcium release - you could start from those linked Wikipedia articles.

I wouldn't really make these a fourth category, they should either be thought of as voltage-gated channels that are modulated by intracellular calcium, or as ligand-gated channels - the ligand just happens to be a calcium ion.

Some channels in this category are not influenced by calcium directly but via calmodulin, which is a common mediator of calcium-driven intracellular influences.


How can birds keep their eyes moist during flight?

Because the nictitating membrane secretes a fluid that is resistant to evaporation. Therefore, birds need not blink their eyes during flight.


How does gene editing in one cell affect other cells?

Gene editing is not done on a single cell but a bunch of cells. However, it still does not affect all the cells. Gene editing/therapy for the entire organism works in these cases:

Stem cells are edited, which give rise to many other somatic cells. Usually done in case of gene therapy in which the stem cells are obtained from the patient, edited and re-implanted.
Some embryonic cells are edited and reimplanted in the developing embryo which gives rise to what is known as a chimeric organism (some cells in the body carry the edit while others don't). Now some of the edited cells will give rise to germ cells which in turn give rise to gametes. In the next round of breeding the chimeric parents would give rise to a fully transgenic (with edited gene) organism.
For unicellular organisms, it is pretty obvious: you just use a selection marker or extensive screening to select for the cells carrying the edited gene.


Not any time soon.  By far the greatest challenge is getting the DNA sequence from the computer into a form that could be implanted into an embryo.  Craig Venter's team was able to build a bacterial genome from scratch, but that was incredibly painstaking work, requiring the assembly of many small fragments of DNA into a single circular chromosome.  With current technology that process becomes prohibitively difficult for a human-like genome.  You would have to build each chromosome from scratch, these chromosomes are linear, and you'd need to associate with them the various histones and other proteins help tightly fold them together.

Another huge problem is epigenetics.  The next generation sequencing methods used for the neanderthal genome just give you DNA sequences, not what epigenetic modifications are present on that DNA.  Genomic imprinting in mammals is very important, and presents problems even in normal cloning efforts where genomes are taken wholesale from live animals.

Not to mention that 1% of the current genome is contaminated with human DNA (not meant as a criticism, its amazing what they have been able to do with a toe bone if this work stands up to peer review).

And none of this takes into account the ethical problems associated with this.  Would you clone it in a human?  Chimp?  Either way its got serious ethical questions.

Dont take my word for it though, here is the leader of the project commenting on this question a few years ago:

  Paabo said because the Neanderthal DNA was scattered in imperfect
  fossils, the notion of cloning a Neanderthal was far-fetched.

  "Starting from the DNA extracted from a fossil, it is and will remain
  impossible," he said. "There is not really an improvement on current
  technologies that would make that possible.


Which was the first DNA-based genome to be sequenced?

Expanding the question to the history of the sequencing of genes and genomes in general, I present a timeline taken from a review by Giani et al., entitled “Long walk to genomics: History and current approaches to genome sequencing and assembly”.

The graphic shows how the size of sequenced genes and genomes has increased since 1965, which reflects developments in sequencing technology that are discussed in this and other articles which may be more accessible. It should be noted that the more modern methodologies are not intrinsically more accurate than earlier ones, but can be employed more rapidly.
I see no value in the “Guinness Book of Records” approach to biology, but to satisfy the poster, the genome of bacteriophage φX174 was the first DNA genome to be sequenced (1977), and that of H.influenzae the first bacterial genome to be sequenced (1995). But the RNA genome of my old friend bacteriophage MS2, was the first genome to be sequenced (1976).
And the first human chromosome to be completely sequenced is not on the graphic as it was only published in Nature a few weeks ago (July 2020) — chromosome X.

Postscript
For the record, the quotation from the whole genome sequencing article is actually a caption for a (gratuitous) image of the bacterium, is unqualified, and, thus, is incorrect. But when reading Wikipedia articles it should be born in mind that they are written by people like you and me. Anyone can edit them, and nobody need check them or correct them. Peer-reviewed papers can also have mistakes, but where they are of this type, the referees should pick them up. (But by the time you read this I will have edited the Wikipedia article.)


How long can one leave sample in lysis buffer for DNA extraction?

It should be fine. Unless they have been contaminated with DNase, none of the components will damage or denature DNA. I've left purified plasmid DNA on the bench for weeks with no apparent degradation, so you should be okay (not that I recommend doing that on a regular basis). I would continue with the purification, according to your professor's recommendation, because you've already come this far. If worst comes to worst, you won't get anything, and you'll have to re-purify. However, the chances of your getting something are pretty high, so you may as well go with it.


Does anyone know of any resources that detail an extensive number of receptor types, their effects, and signalling pathways?

From the comment section:

The IUPHAR database is one of the most extensive database for receptors and ligands. It also contains a lot of additional information and direct references to the literature.


Does aneuploidy include the loss of chromosome arms?

To my knowledge aneuploidy regards to chromosome numerical change, not to losses within chromosomes.
Take a look at this paragraph from An Introduction to Genetic Analysis. 7th edition (Griffiths AJF, Miller JH, Suzuki DT, et al. New York: W. H. Freeman; 2000.)

  Aneuploidy is the second major category of chromosome mutations in
  which chromosome number is abnormal. An aneuploid is an individual
  organism whose chromosome number differs from the wild type by part of
  a chromosome set. Generally, the aneuploid chromosome set differs from
  wild type by only one or a small number of chromosomes. Aneuploids can
  have a chromosome number either greater or smaller than that of the
  wild type. Aneuploid nomenclature is based on the number of copies of
  the specific chromosome in the aneuploid state. For example, the
  aneuploid condition 2n − 1 is called monosomic (meaning “one
  chromosome”) because only one copy of some specific chromosome is
  present instead of the usual two found in its diploid progenitor. The
  aneuploid 2n + 1 is called trisomic,2n − 2 is nullisomic, and n + 1 is
  disomic.

This term (aneuploidy) was coined by Gunnar Täckholm in 1922, and if you want to check the original description you can just look for his original paper:

Täckholm, G. Zytologische Studien über die Gattung Rosa. Acta Hort. Berg. 7, 97–381 (in German) (1922).


Sensory adaptation regarding smell and hearing

Adaptation occurs in every sensory system. For example in vision there is the motion after effect that occurs through adaptation of visual neurons in the cortex. Also, the visual system strongly adapts to low and high lighting conditions through light and dark adaptation. The tactile system also shows substantial adaptation, as touch receptors in the skin fail to convey information after prolonged stimulation (you won't feel a watch/ring/band aid etc after wearing it for a while). For example, mechanoreceptors in the skin such as the Pacinian corpuscles fail to transmit tactile stimuli when activated for a prolonged time. The auditory system also adapts to loud sounds by cortical mechanisms as well as  peripheral mechanisms through the middle ear muscles. Lastly, as you correctly identified, the olfactory system adapts to stimulation as well through metabolic mechanisms that decrease the responsiveness of chemical receptors. The list of adaptational mechanisms provided is not comprehensive, but I just used some obvious examples to show that adaptation occurs in all the senses in a variety of ways. In fact, one of the hallmarks of any physiological intact sensory system is the capability to operate over a wide range of stimulus levels. For example, vision operates over a range of intensities differing 8 orders of magnitude, while hearing operates in an intensity range of 1013. To maintain such an impressive range of input intensities sensory systems have to adapt at various levels. As an analogy, the same applies to your photo camera in which the exposure time has to be regulated in order to take pictures under different lighting conditions.

So to come back to your suggestion that smell cannot be revived after continued stimulation while it can be revived with other senses is not true I think. The attentional revival you are talking about is not so much adaptation but has more to do with the attentional shift, which may occur with any sensory modality.


What is the difference between options protein and replication in the NCBI database?

Interactions denote protein-protein interactions, which means physical association between proteins. By nature, these networks/graphs are undirected.

Replication interactions (actually a not very good term) denote gene regulatory interactions that affect HIV replication. These sets also include the regulatory effects of HIV genes on host genes (and hence the terminology is unsuitable). These networks are directed as well as signed (positive or negative interactions i.e. activation or inhibition respectively).

You can see for yourself, from the dropdown boxes and the interaction lists in this page.


How does consumption of vinegar affect food chemistry?

In the case you're talking about (just using vinegar to taste), there should be no effect whatsoever on a healthy stomach. The stomach already contains a significant amount of acid, and a little bit more from the acetic acid in vinegar won't change much, just like eating some citrus fruit with a meal (oranges, lemons, and whatnot) won't change much. Acid-mediated hydrolysis of chewed food is only the first of many steps in digestion - a significant portion is performed by enzymes and commensal microorganisms in the gut. Changing the type or amount of acid by a small amount won't affect anything significantly in the long run.

The only exception I can think of is for people suffering from peptic ulcers, whether from over-use of NSAIDs (Non-Steroidal Anti-Inflammatory Drugs such as aspirin, ibuprofen, naproxen, etc.), infection with H. pylori, or possible genetic/developmental issues (most often seen in young children). In these cases, consuming an overly-acidic meal may aggravate the symptoms of peptic ulceration.


Why do we have to exhale (or inhale) in order to speak?

As part of your question, you ask if other animals can create sound without continuous airflow. Many insects (e.g. cicadas and moths) do exactly this by using tymbals. A tymbal/timbal is an external membrane organ that is controlled by muscles or wing movements, that cause the membrane to flip back and forth, creating clicks or other sounds. So in many ways it produces sound in a similar way as loudspeakers, by creating sounds using a vibrating membrane.

One example can be found in this clip, which nicely shows how the organ functions:
Moth Making Sonar Jamming Sounds (youtube)

On this page (in Swedish) you can also listen to slowed-down butterfly sounds from four species.


Deliberately choosing one nostril to breath through

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3681046/
Assessment of the Effects of Pranayama/Alternate Nostril Breathing on the Parasympathetic Nervous System in Young Adults
Result and Conclusion: This study showed that the parasympathetic tone was enhanced appreciably in the participants. The observations of this study suggest that the yogic exercise of A.N.B. influences the parasympathetic nervous system significantly.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3978938/
Slow Yogic Breathing Through Right and Left Nostril Influences Sympathovagal Balance, Heart Rate Variability, and Cardiovascular Risks in Young Adults
Short-term practice of LNB improves vagal tone, increases HRV, and promotes cardiovascular health of medical students. Practice of RNB increases sympathetic tone and could jeopardize cardiovascular health.

There seems to be some evidence that this works.


Genomic library preparation: Why does the restriction enzyme not cut into the gene?

A genomic library is generated for the purpose of encapsulating the full genetic component of an organism.
You do this by fragmenting the genome with  restriction enzyme that cuts at its recognition sequence. These fragments are then taken and cloned into a plasmid, so that they can then be sequenced inside the plasmid using common sequences that are found on the plasmid but not (generally) in the organism itself. The sequencing would traditionally be performed by Sanger sequencing, which has a limit to how long a sequence you can do at once - really good sequencing will get you ~1000 bp, with sequence quality tailing off after about 600 bp.
The genomic library are not intended for expression - once genes are identified, they can be sub-cloned into an expression plasmid to see what they do. So for this purpose, cutting a gene into fragments isn't a problem, as you will find the rest on another plasmid and can re-construct the full-length gene by taking the two fragments and assembling them.
The reason you use the restriction enzyme is that the sequence that it cuts at is also used for inserting it into the plasmid.
So, at this point you might be asking yourself how do you match the ends of genes (or any sequence for that matter), when they are all cut by an identical sequence?
Well, the answer that is that you use multiple restriction enzymes, either by themselves or in combinations to generate a variety of fragments cut at different sites. This will mean that once you create the libraries from these different digestions, you can sequence through the different libraries and find where the fragments overlap, and then assemble all the sequences together into the original sequence.
For instance if you look at the picture below. If you imagine the the black boxes  are the same gene, and the in the top one is cut with restriction enzyme A and the bottom with B, you can see that the two restriction enzymes generate overlapping fragments, so if you sequence the fragments from both restriction enzymes, you can find where the ends in A match others in A, by looking at the fragments in B.


Why not use SDS-PAGE as a method to detect viruses?

Put simply, the answer is that you could seek to detect viral proteins, but because these proteins would be very minor components of your sample, you would have to use an immunoblotting technique to detect a specific viral protein. While immunoblotting is quite a sensitive technique, I think its fair to say that it can be technically demanding. In contrast a PCR reaction is exquisitely sensitive and is fairly robust. PCR is also technically more staightfoward because DNA is generally easier to work with than are proteins.

Before the advent of PCR, immunoblotting would have been the method of choice.


Can the Quarternary Extinction event be linked to the spread of mankind around the world?

Only in islands can this hypothesis be supported.  But islands are NOT continents, and that raises problems with the hypothesis.  The most inconspicuous of which is timing.

In Australia, the gap between man setting foot on Australia and the extinction of Australia's megafauna was 17,000 years. Too long.

Man left Africa and set foot in Eurasia more or less than 50,000 years ago, yet the extinction of Eurasia's megafauna happened 10,000 years ago. Too long.

The oldest discovered American, "Eve", was discovered in a cave in Mexico's Yucatan Peninsula and dated to be 13,500 years old, 500 years older than the supposed time that man crossed Beringia. This could imply that man crossed Beringia at a far earlier date, yet the dating of the extinction of America's megafauna coincided with that in Eurasia. Too long.

There's also into consideration the Younger Dryas climate chaos phenomenon, which did coincide with the extinction of the 30 genera of Pleistocene megafauna, a handful of microfauna and plants, not to mention the Clovis culture itself.

If man was the cause of the extinction event, the gap between man setting foot in new lands and the megafaunal extinction would've been a few generations, not a few millennia.


Cross-integration of puma subspecies populations

The study you are referring to is probably a study by Culver et al. (2000). They performed a genetic analysis of 315 individuals of the American Puma (Puma concolor), also known as the cougar. Their thorough analysis (especially for the late 1990s) showed that the Florida panther and the western North American pumas were the same subspecies, Puma concolor couguar (note the proper spelling of the subpecies). All individuals north of Nicaragua are this subspecies. From Nicaragua south into South America, they recognized five additional subspecies of American Puma.  The distribution of the subspecies, as well as the sample locations, are shown in the figure below, taken from Culver et al. (2000).

Notice in the figure above that the American Puma used to occupy most of North America but now is restricted to the the region west of the Rocky Mountains, except for the isolated Florida population. Because the genetics of the Florida Panther and the western American Puma are effectively the same, individuals from the western US can be introduced into southern Florida. This idea was first proposed (to my knowledge) by Hedrick (1995) as a conservation measure by introducing genetic variation and reduce the effects of inbreeding. In that same year, eight female pumas were transferred to Florida from Texas, which had the population of panthers closest to Florida. Introducing pumas from outside of Florida has pros and cons, reviewed by Pimm et al. (2005), from both a short-term conservation perspective as well as long-term evolutionary perspectives.

Several years after the Texas pumas were introduced, Johnson et al. (2010) performed a genetic analysis of the Florida population. They showed that the Texas females were indeed reproducing in Florida. The release of Texas panthers did introduce more genetic variation into the Florida population and reduce the effects of inbreeding. The net effect was that more Florida panthers were surviving. The downside is that habitat loss continues and the effective population size is still very small. That means that inbreeding is still very much an issue.

The studies to date have focused on genetic integration and overall recovery due to the introduction of genetic variation but I did not find any studies that reported any behavioral changes since the 1995 introduction. Given that it was only 8 females, I would not expect any significantly different behaviors to be introduced into the Florida population.

Introducing more genetic variation from Texas (and perhaps populations farther west) may be helpful but ultimately preservation of habitat and improving ability of individuals to move among available habitat fragments via corridors is necessary to protect the species long term.

Citations

Culver, M. et al. 2000. Genetic ancestry of the American Puma (Puma concolor). Journal of Heredity 91: 186-197. (open access)

Hedrick, P.W. 1995. Gene flow and genetic restoration: The Florida panther as a case study. Journal of Conservation Biology 9: 996-1007.

Johnson, W.E. et al. 2010. Genetic restoration of the Florida Panther. Science 329: 1641-1645.

Pimm, S.L. et al. 2005. The genetic rescue of the Florida panther. Animal Conservatation 9: 115-122. This issue of Animal Conservation has a few articles dedicated to the Florida Panther.


Are all endocrine glands associated with common human feelings?

You may not be able to feel or be aware of the actions of all endocrine glands at the time they occur.

The parathyroid gland secretes parathormone, which affects calcium absorption in the intestine, kidneys and bones, phosphate excretion in the kidneys and vitamin D production in the kidneys. I'm not sure if one can feel these actions or its consequences.

The adrenal cortex secretes aldosterone, which maintains sodium and potassium blood levels, which is related to blood pressure and urine excretion. It also secretes cortisol, which affects glucose utilization, fat breakdown and inflammation and affects the actions of some other hormones, but within normal physiological range, you don't feel these effects. Cortisol is also known as a stress hormone, but its actions are much more subtle (on the level of metabolism) than those of adrenaline (heart rate, excitement). Saying that, cortisol secretion can be related to sleep and appetite. There is a lot of speculation how it might affect mood or "energy levels" (adrenal fatigue).

There are many gastrointestinal hormones (gastrin, secretin, cholecystokinin, ghrelin), some of which affect digestion, some peristalsis and some appetite and you may not be consciously aware of all of that.

Some pituitary gland hormones (ACTH, TSH, FSH, LH) stimulate the secretion of hormones from other glands (adrenal, thyroid, gonades) and some (growth hormone, ADH, oxytocin) act directly on organs - I don't think you can say that you can feel these effects.

Some hormones have effects on other hormones (cortisol > adrenaline ; thyroxine > growth hormone, etc.), so it may not always be possible to pinpoint which feeling is directly related to which hormone.

Common human feelings related to hormone secretion:

Excitement or stress response, including fast heart rate and breathing and anxiety: short term response: adrenaline; long-term response: cortisol
Appetite: ghrelin, leptin, adiponectin, cholecystokinin, insulin, glucagon-like peptide, gastrointestinal peptide...
Sexual drive: sex hormones, mainly testosterone and estradiol
Sleepiness: melatonin, cortisol
Depression: cortisol, sex hormones (mainly in women)

The point of this answer is to show that some of your feelings can be simply affected by hormones, which are note some ultimate forces, and that being aware of that can help you to control them to some extent.


List of heritability estimates in humans?

You may consider consulting the H2DB database. The database is quite new, so the number of heritability estimates is not very high at the moment (currently 225 estimates for human, 838 estimates in total), but it's a start. The database is described in a paper by Kaminuma et al.(2)


If a species has a vestigial anatomical structure that it no longer uses, it may or may not disapear through natural selection.

Evolution is based on four mechanisms :
- mutation
- natural selection
- sexual selection
- genetic drift

A no longer used structure can disapear if a mutation makes it to. Then, if it confers a selection advantage (natural or sexual), then individuals without that structure will survive and / or reproduce better than the other. The mutation will spread among the population and structure may finally disapear.

If it does not confer benefit the individual nor decrease it's chances of survival or reproduce compare to others, mutation may or may not be conserved and so for the structure.

Genetic drift can accelerate disapearance of a structure, especially if the population is really small, even if it does not confer any advantages to the individuals. The mutation can rapidly spread through the population just by chance.

For example, in human body, the appendix is no longer used but still remains. It's absence does increase chance of survivol nor is attractive to sexual partners, so it doesn't imply natural or sexual selection structure. Genetic drift may or may not randomly make it disapear one day, no one knows.


Why do some reflex actions involve interneurons, but some don't?

I did not realize it but the knee jerk reflex is a stretch reflex and thus only involves two neurons (monosynaptic). Many many more reflexes use 3 or more neurons (polysynaptic) so include interneurons.

monosynaptic are common for muscle stretch limiting reflexes, that is why I knew them by their more common name stretch reflexes and did not make the connection. They don't involve interneurons becasue they would offer little benefit, they are self regulating most of the time and only involve a single source and a single destination and will not see much benefit from modification of the signal.

This slideshare on reflexes can provide some detailed information and a place to keep researching from.


I've done a functional annotation of a non-model, and used Blast2Go with fine results.

Specifically, I took all of my proteins and queried again the NCBI non redundant (nr) protein database using mpiBLAST, then I analyzed this output using Blast2GO (B2G4PIPE) and a local B2G Database.


What physiological processes within a muscle cause the latent period in a muscle fiber?

The action potential causes Ca2+ ions to be released in the cells, that is needed for muscle fiber contraction. There is a small time delay from the arrival of the action-potential until the Ca-ions are released and reach the required concentration in the cell for contraction. On the molecular level there is a protein called troponin (this is bacically located on the actin filament along with tropomyosin and obscures the myosin binding site(s)), that bind calcium and then undergoes conformational change - this also adds up to the delay. After this - the conformational change of troponin - myosin and actin can bind together and contraction can occur through conformational changes. All these binding and conformation changes take a small time to be completed, and thus causes a small delay. Below is a picture about the molecular mechanism ofof muscle contraction taken from this wiki page. The linked wiki page has real good detailed information.

I found this article and where they exactly measured things. To clarify my answer (taken from the linked article):

  Electromechanical delay (EMD) was described as a time elapse between the onset of muscle electrical activation and onset of force production, reflecting both electrochemical processes [i.e., synaptic transmission, propagation of the action potential, excitation-contraction (EC) coupling] and mechanical processes [i.e., force transmission along the active and passive parts of the series elastic components (SECs)]

So as for the whole muscle, not for just one cell the delay is caused by the things listed in the above quote - although excitation-contraction (EC) coupling and force transmission (things I have described earlier) take place in every single muscle cell that is in a specific muscle fiber.

Edit 2: I found a good and simple ppt/pdf about AP propagation and muscle contraction here.