A theory about the possible connection between protists and first animalia

Short Answer:

Probably the most widely accepted (though certainly not fully accepted) theory of animal evolution is called the Colonial theory.

According to the Colonial theory of animal origins, the earliest animals (i.e., sponges) seem to have arisen from colonial protists called choanoflagellates forming an invaginated hollow, spherical colony.

However, other theories do exist: Syncytial Theory and the Synzoospore Theory (proposed by Mikhailov et al. (2009)1)

Regardless of these theories, no reasonable theory about the evolution of animals from protists would link such evolution to "microanimals" given that microanimals (as defined by the OP) is not a phylogenetic group but rather a term to describe microscopic animals from various taxonomic groups.

 Long Answer:

There seems to be strong morphological evidence that choanoflagellates are the closest protist relative to currently living animals -- specifically to the simplest group of animals: the sponges (phylum Porifera).

 Protist / Animal phylogeny, Source: Cengage 20132

Specifically, we can see very similar characteristics between a choanoflagellate and a choanocyte (or "collar cell") of a sponge.

The choanoflagellates often form colonies consisting of numerous protists adhering to one another using adhesion proteins.

Due to the morphological similarities between choanoflagellates and choanocytes of sponges (along with similarities in adhesion proteins and signaling proteins shared between both), and the regular colony-forming tendencies of choanoflaggelates, it has been long suspected that the evolution of multicellular animals arose from these protists.

Ernst Haeckel (1874) was the first to propose that colony-forming chonaoflaggelates were the precursor to modern animals in a theory he called the Gastraea theory and which is now called the Colonial Theory of animal evolution. This thoery is summarized simply by Mikhailov et al. (2009)1:

  According to Ernst Haeckel, the transition from unicellularity to multicellularity
  proceeded through two consecutive stages (Fig. 1A). First, unicellular flagellates aggregated to form a hollow ballshaped floating colony of identical cells. This hypothetical stage was named the Blastaea to reflect its similarity with the blastula, an early stage in animal embryogenesis....

  ...At the second stage, the homogenous cellular wall of the Blastaea invaginated to form a second layer, the precursor of the primary gut. After this important event the Blastaea acquired primary cell differentiation (=spatial cell differentiation).

  Haeckel named this hypothetical ancestral form the Gastraea, again to indicate its similarity with the gastrula stage in animal embryogenesis. According to Haeckel, extant
  cnidarians and sponges are the first direct descendants of the ancestral Gastraea,(11) because their body plans derive from two embryonic layers.

Below is an illustration of the Colonial Theory of animal origins:

Other Theories:

I've cited two additional theories at the start of this answer (i.e., the Syncytial Theory and the Synzoospore Theory proposed by Mikhailov et al. (2009)1). For the sake of breviy, I will exclude further discussion of either theory here. Please feel free to visit my links/citations to learn more. I certaily encourage other users to provide answers describing such theories in more detail if they find doing so necessary and insightful for this post.

Regarding Microanimals

The term "microanimals" is simply referring to the size of the organism (i.e., that they need magnification for viewing) and not to any phylogenetic or evolutionary connection between these microscopic animals. Put differently, microscopic animals actually belong to a broad range of animal phyla -- in other words, they are not immediately related.

the Wikipedia post the OP links to (and the one I also link to in the preceding paragraph) lists, for example, microanimals from the phyla Arthropoda, Rotifera, and Loricifera.

Given this information, I strongly doubt you will find a theory suggesting that "microanimals" (as defined) played a role in the transition from protists to Animals.

1. Mikhailov, K.V., Konstantinova, A.V., Nikitin, M.A., Troshin, P.V., Rusin, L.Y., Lyubetsky, V.A., Panchin, Y.V., Mylnikov, A.P., Moroz, L.L., Kumar, S. and Aleoshin, V.V., 2009. The origin of Metazoa: a transition from temporal to spatial cell differentiation. Bioessays, 31(7), pp.758-768.

2. Starr, C., Taggart, R. and Evers, C., 2013. Biology: The unity and diversity of life. Cengage Learning.


Why is DNA replication not 100% accurate

Nothing is 100% precise - any measurement or process allow for some error, the only difference is how often such errors occur (i.e., the probability of an error). These wildely range in biology - e.g., it is about 1 per $10^4$ in HIV replication, but only 1 per $10^9$ for human DNA (due to the repair mechanisms).
Note that $1$ in $10^9$ for human DNA means pretty much that there is about 1 error per each copying of the genome (which has the size of about $3\times10^9$). One could therefore still pose a question of why the error rate is so high? E.g., Human body consists of about $15\times10^{12}$ cells. Thus, if the error rate were about 1 per $10^{22}$($\approx 3\times10^9$ by $15\times10^{12}$), we could have human organisms consisting of the cells with identical DNA.
The answer to this is that errors are not necessarily bad: the copying errors are the source of the mutations driving the evolution! Note also that many of the errors have no effect at all on the well-being of the organism. Thus, it is fair to say that the existing error rates were selected by the evolution for assuring the appropriate rate of the evolutionary change/adaptation, without causing immediate harm to the organism. (One could even speculate that 1 error per genome copy is the appropriate rate across the organisms, but for a moment I cannot support this assertion by references).


What are the evolutionary niches differentiating an apple from a pear?

I wouldn't be suprised if no one has hard data on this. In any case there is more than one answer to this question.

Niches are defined more than one way.

In the narrowest definition, the niche might be defined as the ability of the different trees to grow in different terrains or be eaten by different animals in the same environment.  I can't comment on that, but in most environments, there is in practice little difference between the two.  The classic example of this is Darwin's finches - where a single species eventually becomes many, each specializing in a specific kind of lifestyle (what they eat/where they net) on the islands of the Galapagos where they were situated.

In the broadest definition of niche, they do have a different niche because they are different species, and their differences allow them to be eaten by different people.  In their highly domesticated environs, apples and pears each have a niche defined by the fact that they are both stocked in the produce sections for people to eat as they choose.

Its worth mentioning that Darwin determined that different organisms can inhabit the same niche.  In his case he saw that on different islands of the Galapagos he saw that the finches had evolved into different species, each of which took up the role that a different bird might have back home.  so its possible that apples and pears may have substantially the same niche in their respective evolutionary histories.


Can people with AIDS/HIV be vaccinated?

Yes. Immunization is an important part of the overall treatment strategy for HIV positive individuals. HIV infection is a risk factor for a number of vaccine preventable infectious diseases. Immunization in these patients is particularly important because of their increased risk of developing disease. (See Cecil Medicine Ch 396)
Can the immune system still mount a response to the vaccine?
Yes. HIV infection does lead to a decreased immune response. Though the primary deficiency is a decrease in both CD4+ (helper) T-cell count and function, there is, perhaps consequently, B-cell dysfunction as well. This would suggest that vaccines are less immunogenic. When this is studied directly, as would be expected, we see that vaccines are less immunogenic, but they are still effective.
Which vaccines are given?
Specific recommendations are based on both the age of the individual and their immune status. As a rule, vaccines are more effective when given early in the natural history of an HIV infection or after immune reconstitution with HAART, but there is some effectiveness and little risk of heat killed or subunit only vaccines even in highly immunosuppressed individuals. While live attenuated vaccines are contraindicated in individuals with a CD4+ cell count below 200, these vaccines are given routinely to other HIV positive patients. Current guidelines are found here. Here is the main figure from those guidelines:


Can I ask tip for tissue measuring(especially for RNA preparation)?

I do not have specific experience with liver tissue, but here I would do a couple of things. First, to get around your issues with weighing tissue, set an acceptable range around 20 (say, plus or minus 5mg, so ranging from 15 to 25mg) and then normalize your RNA yield to that starting weight. Second, look into ways to preserve the RNA in your tissue as you're processing it. You could try RNAlater solutions or other chemical means of stopping RNA degradation, or just snap freeze your tissue in liquid nitrogen. Good luck!


Does muscle get bigger by increase in size of individual cells or increase in number?

The "back of your mind" is correct: "if the muscle gets bigger, it's simply because individual cells get bigger."

Growth of muscle can occur in three ways:

by an increase in muscle cell numbers
by an increase in muscle fiber diameter
by an increase in fiber length.

However, growth in cell numbers is limited to the prenatal and immediately postnatal period, with the animals and man being born with or soon reaching their full complement of muscle cells.

  [G]rowth occurs by either hypertrophy of the existing muscle fibers by adding additional myofibrils to increase the muscle mass or by adding new sarcomeres to the ends of the existing muscle fibers to increase their length. Both of these mechanisms occur during the growth process. Growth in the girth of the muscle fibers... may be stimulated by development of stress creating an unequal pressure with splitting at the Z-band and development of additional SR and T-tubule systems. This adds to the diameter or girth of myofibers without any hyperplasia. The growth in length occurs at either end of the fibers and results in addition of new sarcomeres. In both cases, new myofibrillar protein must be synthesized and deposited in the muscle cells.

Adding or removing sarcomeres and myofibrils is determined by exercise, that is, the degree of force a muscle can generate which is in turn dependent on the degree of overlap of the thick and thin filaments. Thus, the amount of tension would control the number of in-series sarcomeres and the number of myofibrils in a single muscle fiber.

Nutrition is also known to play an important role in muscle growth, but growth (that is, increase in girth) cannot occur without exercise.

The exact roles of GF and IGF-I are not completely clear.

Muscle size does not increase by the addition of new muscle cells:

  The results show that the increase in muscle cross-sectional area from childhood to adult age is caused by an increase in mean fiber size. This is accompanied by a functional development of the fiber population: the proportion of type 2 fibers increases significantly from the age of 5 (approx. 35%) to the age of 20 (approx. 50%), which, in the absence of any discernible effect on the total number of fibers, is most likely caused by a transformation of type 1 to type 2 fibers.

Activation of satellite cells, a claim made by body builders, is mis-represented by them. The satellite cells seem only to aid severely damaged muscle cells to heal, not to increase in number.

Muscle growth and exercise
Muscle hypertrophy
Growth and development of human muscle: A quantitative morphological study of whole vastus lateralis from childhood to adult age
Regulation of muscle mass by growth hormone and IGF-I


Which part of the brain needs to be shut down to lose conciousness?

There is no widely-accepted neurological structure that mediates 'consciousness.' Even if some structures have been shown to be necessary for consciousness, they have not been shown to be sufficient. This is true with anesthetic mechanisms as well -- their ability to paralyze and block pain signals is fairly well-understood, but the mechanism of loss-of-consciousness is still unknown.

Still, 'consciousness' has to be there, somewhere between being awake and being dead, states which anesthetics can readily bridge (review):

  Nevertheless, at some level of anesthesia between behavioral unresponsiveness and the induction of a flat EEG [indicating the cessation of the brain’s electrical activity, one of the criteria for brain death (22)], consciousness must vanish.

Later in the same review:

  The evidence from anesthesia and sleep states (Fig. 2–3) converges to suggest that loss of consciousness is associated with a breakdown of cortical connectivity and thus of integration, or with a collapse of the repertoire of cortical activity patterns and thus of information (Fig. 2). Why should this be the case? A recent theory suggests a principled reason: information and integration may be the very essence of consciousness (52).

This is consistent with my own take. Consciousness itself is the subjective experience of 'brain,' so it can't be lost, just poorly integrated.


Estimates of historical human population size

Although I cannot find the Scientific American article to which the poster refers, I assume that the “historic human population size” is the size of the human population in Africa before it underwent the expansion that accompanied the emergence from the African continent. Some important papers on this subject were published in the late 1990s (somewhat later than 30 years ago) and there is a suggestion in one of earlier estimates that I have not yet found a reference for.

There is an implication in the Harpending et al. paper (below) of earlier estimates of the order of 1,000. I will try to find the source (help on this welcomed).

Harpending et al. published a paper in PNAS of February 1998 in which they conclude an effective population size of the order of 10,000 individuals for most of the Pleistocene.

Reich and Goldstein published a paper in PNAS of July 1998 in which they conclude a maximum pre-expansion population size of 5,900.

A more recent study by Huff et al. published in PNAS in February 2010in which they estimated that the effective population size of human ancestors living before 1.2 million years ago was 18,500, and in which they rejected all models where the ancient effective population size was larger than 26,000

Why should the later estimate be more likely than the earlier ones?
Although the details of the calculations are complex (or at least too complex for me), it appears that the genetic markers that are used are crucial, and that it is important to have markers that represent rare mutational events. The earliest studies apparently used mitochondrial genes and the non-combining parts of the Y chromosome as markers. (These are used and are valid for studies of more recent time.) The limitations in these resulted in a shift to Alu repeats and microsatellites in the two 1998 papers, respectively. The 2010 paper used the insertion of the longer LINE repeats, which occur about one tenth as often as Alu insertions.
There is a Wikipedia article on this topic that may be also be of interest.


What does (G+) (G++) in terms of male mutation rate and male-heterogametic XY-system?

I think you need to provide more context.  When I saw G++, my first thought was the C++ compiler of that name.  I am unaware of any universal use for the term in biology.  It could very well be context specific.  It is common to use that sort of notation when describing alleles in a population, with the pluses following whatever variable name you gave to the allele.  So if we had an allele that we called G, and an individual had two copies of that allele, it would be common to see that individual referred to as G++, with G+ being used to refer to someone with only one copy.  I think it is quite possible that this is what the term means in your context but it is impossible to say for sure without more information on what the question you are being asked is in reference to.  Maybe it would help if you posted questions 1-4 or the blurb that precedes the problem set so we could see what you are actually being asked.


The first picture is an Icterine warbler. Because of the yellowish plumage (never in the eastern olivaceous) and the with fringes of tertiary characteristic of the species and never present in the genus Phylloscopus. Also the color of the leg, greish-bluish is quite specific of the Icterine.

The second and third picture are of a Willow warbler (Phylloscopus trochilus). The legs are pale compared to a chiffchaff and the primary projection (the length of the primaries that pass the tertiary) is extremely long and very typical of the willow warbler. You can see the difference in the image below.
 Here a useful webpage


This article covers your desires. Briefly, the single species that weights the most is the cow (520 million tonnes in 2011, now probably way more). About the most members, it looks like that the prize could go to the Antarctic krill (7.8 x 10^14 according to Wikipedia. [

This BBC article, instead, argues that collembola might be the most numerous group on Earth, being present in the number of 10000 per square meter (I leave the calculation to the reader). Collembola, however, are made up of ~6000 species. The same goes for ants and termites.

Regarding bacteria, the same article mentions
cyanobacteria, and more interestingly Wolbachia, an intracytoplasmic parasite that can bend the sex of the progeny of its host to spread more effectively.


Meaning of arrows in 3D representation of proteins

The flat arrows are a cartoon representation of β-strands (one type of regular hydrogen-bonded secondary structure). The direction of the arrow is the direction of the amino acid sequence (arrow head pointing towards the C-terminus).

The thin wires are regions with no regular structure.

There are also two small green spiral ribbons in the foreground left and right, which represent α-helices (the other main regular secondary structure).


Genetic variation and sensitivity of wild cabbage

I am going to assume that Kale is a plant derived from wild cabbage and has been selected upon for certain attributes by humans for 1000's of generations.

1 There are two principle reasons why genetic (allelic) diversity might be lower in the kale subgroup than in the wild cabbage. Firstly, strong selection imposed by humans may have diminished allelic diversity. Strong selection can drive alleles to fixation. Secondly, if the kale has come from a small sub-population of the wild cabbage it may have been through a genetic bottleneck, this is likely to reduce allelic diversity because, unless all alleles from the original population are captured in the founder populations, some alleles will be lost by genetic drift.

2 Generally allelic diversity is a "good" thing in an unstable environment. It allows different trait combinations and variation in traits to occur. If the environment changes drastically then it could impose severe selective forces on the population, those with high allelic diversity are likely to come up with a combination of alleles that survives.

E.g. Humans only allow the cabbages over 18cm in diameter to reproduce in to the next generation. 5 loci affect cabbage size, each having a "large cabbage" (C) allele and a "small cabbage" (c) allele. Having 5 c alleles gives a cabbage size of 15cm. Each C allele adds 1cm. If a population has fixed the c allele at 3 loci (i.e. there is low genetic diversity) then none of the cabbages will be >18cm. If a population has both the C and c allele at all loci then some of the population will be over 18cm.

3 The final question is difficult to answer, it depends on what you define as "a good recommendation,"  that is very subjective. If the aim is to maximize allelic diversity then yes, if it is to maximize cabbage size it is probably no (because the "genetically engineered" plants have been selected upon for large cabbages - they might have the C alleles fixed in the populations!)


Powdered meal replacement vs regular meal

Yes you could live off a protein shake type supplement if it had the vitamins, minerals, protein, carbohydrates, and fats you would need. Would you want to? Probably not.

First thing we must determine is the protein whey or soy? If a male is consuming this meal replacement and the only protein is from soy, their estrogen levels will be elevated. In Soy Protein Isolate Increases Urinary Estrogens and the Ratio of 2:16α-Hydroxyestrone in Men at High Risk of Prostate Cancer, Dr.s Jill M. Hamilton-Reeves, Salome A. Rebello, William Thomas, Joel W. Slaton, and Mindy S. Kurzer concluded that soy does elevated estrogen in men which helped with the reduction of prostate cancer [1], but as a male, you wouldn't want to have a lifetime of increased estrogen [2].

Infertility. Estrogen is partly responsible for creating healthy
sperm. When estrogen levels are high, sperm levels in semen may fall.
This can lead to fertility issues.
Gynecomastia. Estrogen may stimulate breast tissue growth. Men with
too much estrogen may start developing larger breasts.
Erectile dysfunction. A balance of both testosterone and estrogen is
important for healthy sexual growth and development. Sexual function
may be impacted when these hormones become imbalanced. Men with high
levels of estrogen may have difficulty getting or maintaining an
erection.

So to be on the safe side, let's assume that the protein is from whey and we have one less thing to worry about. Now as for the vitamins and minerals, the Mayo Clinic states that [3]:

  Supplements aren't intended to be a food substitute because they can't replicate all of the nutrients and benefits of whole foods, such as fruits and vegetables.

and there are three main differences:

Greater nutrition. Whole foods are complex, containing a variety of
the micronutrients your body needs — not just one. An orange, for
example, provides vitamin C plus some beta carotene, calcium and
other nutrients. It's likely these compounds work together to produce
their beneficial effect.
Essential fiber. Whole foods, such as whole grains, fruits,
vegetables and legumes, provide dietary fiber. Most high-fiber foods
are also packed with other essential nutrients. Fiber, as part of a
healthy diet, can help prevent certain diseases, such as type 2
diabetes and heart disease, and it can also help manage constipation.
Protective substances. Whole foods contain other substances important
for good health. Fruits and vegetables, for example, contain
naturally occurring substances called phytochemicals, which may help
protect you against cancer, heart disease, diabetes and high blood
pressure. Many are also good sources of antioxidants — substances
that slow down oxidation, a natural process that leads to cell and
tissue damage.

So you could live off of some meal replacement shake for the rest of your life but should you? Probably not.


Cortical projections from layers 2/3 back to 4?

Excitatory neurons in layer 4 are not all stellate in all cortical areas, for example see Smith and Populin, 2001 who show clearly that in auditory cortex most excitatory cells in layer 4 are pyramidal. There are also many cortical areas that have no clear "layer 4" and also do not contain spiny stellate cells.

In general, intracortical circuitry is not fully understood. Although your question shows understanding of this next point, let me highlight it anyways because it is a point that is often forgotten: neither axons nor dendrites are constrained to the layers containing soma. Therefore, it is possible for a cell of "layer A" to contact a cell of "layer B" even if the "layer A" cell has no axons in "layer B" and the cell of "layer B" has no dendrites in "layer A": they could have axons and dendrites in "layer C", for example.

One approach has been taken by some such as Binzegger et al., 2004 is to estimate intralaminar cortical connectivity based on co-occurrence within a given layer of axons and dendrites. This approach is an approximation, of course, because there is no guarantee that axons contact dendrites randomly within a given layer. For example, axons could preferentially contact the dendrites of inhibitory rather than excitatory cells, and this would fundamentally influence the circuit dynamics.

The result from Binzegger et al (their Figure 1 is a fairly clear summary figure, if you want to start there) is that, although there are some predominant patterns of connectivity, there is no pure feed-forward circuit: all of the connections are at least partially reciprocal. For the example you gave, layer 2/3 to layer 4, the number of connections from layer 2/3 to layer 4 is estimated to be about half as many as the number of connections from layer 4 to layer 2/3.

Figure from Binzegger et al, 2004; Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported License

However, it is also possible that these connections preferentially target inhibitory cells rather than excitatory cells in layer 4: see Thomson et al., 2002.

It is likely that the variety in sources/diagrams you are familiar with is simply because people take different approaches to complex systems (and different approaches may be warranted in different situations). Some people choose to highlight the most salient features, perhaps the strongest layer-to-layer connections, in the hope that this produces an understandable, though simplified, model. Other people choose to highlight the vast complexity, emphasizing all of the smaller details that may actually be important.

For an analogy, a chef is likely to just deal with olive oil. They don't care that olive oil is actually a collection of several fatty acids: it's just olive oil to them, and the importance to them is that olive oil is distinct from another vegetable oil. A biochemist, however, might be interested in the specific fatty acids and might point out that those specific fatty acids are found in all sorts of other oils. Neither one is likely to convince the other that they have the better answer for all purposes.

Neither approach is strictly incorrect or better than the other, until better understanding makes one of the approaches obsolete.

References:

Binzegger, T., Douglas, R. J., & Martin, K. A. (2004). A quantitative map of the circuit of cat primary visual cortex. Journal of Neuroscience, 24(39), 8441-8453.

Smith, P. H., & Populin, L. C. (2001). Fundamental differences between the thalamocortical recipient layers of the cat auditory and visual cortices. Journal of Comparative Neurology, 436(4), 508-519.

Thomson, A. M., West, D. C., Wang, Y., & Bannister, A. P. (2002). Synaptic connections and small circuits involving excitatory and inhibitory neurons in layers 2–5 of adult rat and cat neocortex: triple intracellular recordings and biocytin labelling in vitro. Cerebral cortex, 12(9), 936-953.


Does the energy from ATP hydrolysis vary among different cells?

Yes, the energy from ATP hydrolysis can vary between different cell types and condition, because it depends on several factors. Hence, you will find different values in various textbooks.

First, like any chemical reaction, the free energy $\Delta G$ of ATP hydrolysis depends on the concentrations of the reactants. You can explore different values of $\Delta G$ with this calculation tool. Typical values are [ATP] = 10 mM, [ADP] = 1 mM and [P$_i$] = 20 mM, which gives $\Delta G$ = 42 kJ/mol (10 kcal/mol). But all these concentrations can vary between cells, and there is not much data available on intracellular concentrations in specific cell types. Many textbooks give free energy values denoted $\Delta G^{\circ}{'}$ which are calculated at concentrations of 1M, which is of course completely unphysiological.

In addition, the $\Delta G$ is strongly affected by the concentration of Mg$^{2+}$, because this ion associates with phosphate groups and alters their free energy. It also depends on pH, since the phosphate groups can take up/release protons. If you are interested, an in depth analysis is found here.


What goes wrong in the immune system that leads to autoimmune diseases

Your understanding of the process is basically correct. There are of course a lot more details to it, but that wouldn't be in the scope of the question. Do note that only T cells mature in the thymus (that's where the T comes from ^^), whereas B cells mature in lymph nodes and the spleen.

As for why autoimmunity occurs you also understood the basics, however the devil is in the details: wikipedia does have a much longer list of mechanistically different causes. While its often sufficient to explain immune recognition using 'keys' (T cell receptor / B cell receptor = antibody) and their respective 'locks' (peptides bound to MHC / antigens), the exact process of immune cell activation becomes important in autoimmunity, where cells are wrongly activated. This means that there are many possible points at which the 'security system' of the immune cell maturation can (or rather has to) fail to allow autoimmunity.

As for the cross-reactivity of cells: the difference between the binding of B cells (via antibody/B cell receptor to protein surfaces) and T cells (via T cell receptor to peptide sequences) means that in general T cells are much more likely to show cross reactivity - just because the possibility space of a 10-12aa peptide is much smaller than that of a protein surface (even though the probability is still very low).

Additionally - as stated in the comments to your question - both the immune activation pathway and the issue of cross reactivity, while principally understood, are not 'completely solved'. The immune system is insanely complex just by itself and the addition of interactions with both almost all human proteins AND proteins any kind of pathogen, mean that it will take quite a lot of time until researchers can figure out all the weird quirks caused by the 'wrong' combinations.


How to determine if the amount of manganese chloride will change neural resting potential

For theoretical calculations with other ions, you need to know the concentration and permeability of each of the major ions inside and outside the cell, both with and without the added substance (in your case MnCl2), and then use the Goldman equation/GHK equation to calculate resting potential before and after. Approximations would probably be sufficient.

However, chloride can be a bit complicated because the intracellular chloride concentration can fluctuate with extracellular chloride moreso than the other major ions. Therefore, depending on the sensitivity of your experiment, you may need to perform whole-cell patch clamp recordings to measure the resting potential directly.

If the change in chloride is a small percentage of the total, you can probably consider the influence to be negligible.


The replicator equation vs the Lotka-Volterra equation

The key point is that the first equation is describing frequencies, i.e., $\sum_{i=1}^n x_i = 1$, so there are only $n-1$ degrees of freedom. For instance, if $n=2$ (as in Hawk-Dove), you can totally describe the state of the system with just $x_1$, because $x_2$ is just $x_2=1-x_1$. This constraint is enforced by adjusting $\phi$.

To convert the Lotka-Volterra model to the first equation, define $x_i\equiv y_i/\sum_j y_j$.


How can I change my buffer system for protein purification?

Assuming that your protein can handle being in the new buffer, you have multiple options.

Dialysis will work although you might want to consider using a centrifuge spin filter with a suitable MW cutoff to gradually switch buffer and concentrate the sample. Be aware that some of your protein will stick to the filter, giving a loss of sample.

Alternatively you can perform size exclusion chromatography to switch into the new buffer, but you better be sure that the sample will remain stable or you may clog the column. If you can perform affinity chromatography, you can also opt to change buffer in this step.

You can of course try to start with a Tris based buffer and simply adjust pH by dialysis in a tris buffer with the desired pH. Just make sure that the dialysis volume is large enough to counteract the buffer in the sample.

Instead of using PBS you can also try with TBS (Tris-buffered saline), see wiki for details. https://en.wikipedia.org/wiki/Tris-buffered_saline


Social insects can respond in different ways to nest mates corpses. They can bury them (sometimes "entombing" is used in the literature, especially in honeybees because they can seal cells or use propolis to build tombs), eat them ("cannibalism"), but most often a specialized group of workers takes care of carrying them outside of the nest, far from the colony. Usually the older workers specialize in undertaking behaviors, it has been hypothesized that this allows to reduce the risks of contamination because older workers are already more likely to die or have fewer social interactions than younger members of the colony.

  Sun, Q., & Zhou, X. (2013). Corpse management in social insects. International journal of biological sciences, 9(3), 313.

What social insects do with the corpses wouldn't be a good indicator of emotions, simply because they may bring them back to eat them, or take them away to avoid contamination. Whether insects do experience emotions is a complex topic, the most advanced piece of work on the subject has been done on bumble bees:

  Perry, C. J., Baciadonna, L., & Chittka, L. (2016). Unexpected rewards
  induce dopamine-dependent positive emotion–like state changes in
  bumblebees. Science, 353(6307), 1529-1531.


Group selection, in the extreme, yields eusociality due to the shared fate of the replicators in the group.  In a multicellular sexual organism, this "shared fate" of the "group" is the shared prospect that all replicators (alleles) have for making it into the next generation via the meotic lottery that produces the gamete.  Since they share this prospective fate they have an evolutionary incentive to cooperate in the construction of specialized cells that are, in effect, "sterile caste" members of the total "hive".  Similarly, if it is possible to subject all members of a group of individuals to a shared fate through multiple generations -- they will tend to evolve highly cooperative social structures.  However, one of the confusing aspects of the eusocial insect colonies is whether they evolved to be that way through shared fate of individual organisms, or some variant on the meotic lottery's shared fate of alleles.  The answer appears to be, primarily, that it is a peculiar form of meotic lottery in which the genes of the parents have extended phenotypes in the children that, in essence, parasitically castrate the vast majority of the children to help rear more offspring for the parents -- in particular the queen.  In this respect, one can view the evolution of eusociality in the social insects as a perverse form of individual selection where the genes of, say, the queen, cooperate in constructing not just the queen's body but, also, the entire hive.  The sterile castes are simply extended phenotypes of the queen (and the  drone with which she mates).

See "The Social Conquest of Earth" by E. O. Wilson for an in-depth treatment of eusociality and its evolution as set forth by Nowak et al in their recent paper "The Evolution of Eusociality".  See also "The Extended Phenotype" by Richard Dawkins -- in particular the chapter "Host Phenotypes of Parasite Genes".


What conditions are necessary for HPL (human pancreatic lipase) to activate?

The protein referred to in the question is encoded by gene PNLIP, pancreatic lipase. From this annotation of the protein, I see that there is a signal peptide from amino acids 1 to 16. Thus, this signal peptide must be cleaved before the protein can be active in its digestion of emulsified triacylglyerides.

A paper describes the structural changes induced in human pancreatic lipase by lowering the pH. The secondary structure of the enzyme is stable within a pH range of 3.0 to 6.5. At this pH, a reversible opening of the lid controlling the access to the active site was observed. So, there is another aspect of activation - pH and the ability to open the enzyme lid so that the fat molecule enters the active site.


why is the cleavage in frogs holoblastic and not meroblastic?

Because:

Frog eggs are not yolk-rich. They are mesolecithal, they have an intermediate amount of yolk.
Yolk is concentrated within vegetal pole of the egg. That is why yolk-packed macromeres divide much slower than micromeres on the vegetal pole, which barely contain any yolk.

My sources:

https://kjcscientific.wordpress.com/project-excalibur/
Gilbert's Developmental Biology (2009)


Double mutant analysis with null mutants

What is a double mutant ?

See this image.

In this mutant 1 has one mutation, mutant 2 has another mutation while the double mutant has "double"  or 2 mutations.

Key : A,B means double mutation , A means mutation in A and B means mutation in B.

Types of double mutations

  a)Additive phenotype:  A, B = A + B   Implies that A and
  B function independently and on different processes.
   Eg.  A =
  short roots, B = no root hairs A, B = short roots with no root
  hairs.
  Conclusion: A and B function independently on different
  aspects of root development (A is required for normal root growth
  and B is required for root hair development.

  b) Epistatic phenotype: A, B = either A or B

  i) If A = B = A, B   then epistasis implies that both genes function in the same pathway and that each gene is essential to the process.   Eg. A = short roots, B = short
  roots A, B = short roots.  Both A and B are  required for
  normal growth of roots.

  ii)         If A is opposite in phenotype to B, and A, B = A, then epistasis implies that  A and B are in the
  same pathway and B is a negative regulator of A.   Eg. A = long
  roots, B = short roots A, B = long roots.  A is required to
  suppress root growth and B is a negative regulator of A.

  c)
  Synergistic phenotype: A, B >>> A or B.

  Implies that A and B contribute independently to the same process.   Eg. A = long roots (wt = 2 cm, A = 4 cm)    B =
  long roots (B = 4 cm)  A, B = very long roots (20 cm).  A and
  B negatively control root growth independently of one another and
  are performing partially redundant functions.

When your professor was saying that if A and B are in same pathway and you mutate A and phenotype comes as if both A and B have been mutated, then he was probably referring to the epistatic phenotype.

When he was talking about having a stronger effect by mutating them both, he was talking about Synergistic phenotype.

Source : Double mutant analysis


Short answer
In terms of visual function, the low-tier primary visual cortex and high-tier frontal cortex are inactivated. The activity of the intermediate ventral stream and limbic regions are increased, apparently uncoupling low- and high-level vision processing from the system.

Background
The sleep stage where visualizations (dreaming) occur is called the rapid-eye movement (REM) sleep.

Brain imaging studies have shown pronounced effects of REM sleep on the functioning of the visual system.

In the awake state, the primary visual cortex (V1, or striate cortex) is activated, which is mainly concerned with low-level visual processing such as contrast perception. This cortical region in turn projects to higher-level (extrastriate) regions for more complex processing of visual information.

During REM sleep, however, a selective activation of extrastriate visual cortices is observed. Particularly the ventral processing stream is activated, which is associated with perception and recognition in the awake state (Deubel et al., 1998). Also the limbic and paralimbic regions are active (the emotional brain centers).

Interestingly, activity in the primary visual cortex (V1) is attenuated, as well as the frontal association areas of the brain. V1 is the primary, most 'primitive' visual cortex, while the frontal association areas are the highest-tier cortex that integrates complex perceptual information across perceptual modalities (Braun et al., 1998).

Overall, this pattern suggests a model of REM sleep where visual association cortices and their paralimbic projections may operate as a closed system dissociated from the regions at either end of the visual hierarchy that mediate interactions with the external world (Braun et al., 1998).

References
- Braun et al., Science (1998); 279: 91-5
- Deubel et al., Vis Cognition (1998); 5(1/2), 81–107


differentially expressed genes of the treated with estradiol samples

Pathway analysis can be a little tricky. Because pathway enrichment is estimated from the enrichment of genes (or miRNA or what have you) that participate in overlapping pathways, certain pathways often show up for reasons that may have little to do with your experiment. Cell cycle related pathways, in particular, come up a lot, since so many genes are "cell cycle-related". These papers both go over this phenomenon in more detail. The second one is behind a paywall...sorry for that. If you can't access it, but want to read it, I'm sure we can figure out a way to send a pdf.

I deal with this a lot in my own research. My usual strategy is to make pathway analysis only one part of the overall analysis. How that works exactly depends a lot on the nature of your project. For instance, pathway enrichment could just serve as a sanity check, to see that other results aren't widely off mark. Alternatively, you might want to put other results in the context of some pathway or the other & having pathway enrichment data would naturally be a part of this.

Regarding the question of what exactly starvation means in the context of your results, it's possible that, if this pathway doesn't make sense in the context of your experiment, then it shows up as enriched because more starvation-related genes came up as differentially expressed. The degree to which that means that your cells were undergoing starvation could be debatable. I would bet money that there's significant overlap between starvation-related gene sets and those related to "cellular stress" & "cell death". Cell death is one common response to serum starvation, for instance.

Hope that helps!


GWAS: matched-pairs and logistic regression

My first thought was to suggest a mixed effects model, so I will describe that first. But having had a Google there are models known as "Conditional logistic regression" models in which you can include any data structure as a covariate, which may be more appropriate, but I cannot vouch for them as I haven't used them. I would suggest reading the documentation.

Mixed effects models

I only know how to do this in R (stats language - www.r-project.org), but if you're using PLINK (so presumably also UNIX) R is pretty straightforward.

There are a couple of packages available for mixed effects models, my personal preference is function lme in package nlme (CRAN link). This type of model allows you to specify 2 types of independent variable (e.g. age, BMI, ethnicity... in your case);

Fixed effects - such as age, sex (something that is a phenotype of the samples),
Random effects - such as batch or other "technical" consideration,

This means you can format a model as you would before, but include an additional "random effects" term for your "matched" variable;

model = lme( fixed= outcome ~ exposure + covariate1, random= 1|matched )

.

Conditional logistic regression models

In the survival package for R there is a function called clogit (CRAN link) which seems to do exactly what you want. Although I have never used it myself.

From what I can gather this allows you to run a logistic regression with an additional covariate strata(matched), so your model may look like

model = clogit( outcome ~ exposure + covariate1 + strata(matched) )

.

Disclaimer!

This may not be exactly what you are after, as I'm not familiar with your data, so I would suggest heading over to https://stats.stackexchange.com/ as well, and searching for questions about regression analysis and paired observations - if none answer your question then ask a fresh one.


What biochemical molecule viewer allows for changes in amino acids and resulting tertiary structure?

One application that I am aware of that will do this, as well as much else besides, is Swiss-PDB Viewer aka DeepView. If you go to the site and select User Guide in the left hand tabs you will see a subsection called mutations and following that will tell you what the application can do.


What are the biological mechanisms behind the increase in cancer risk and alcohol consumption?

There aren't many studies which associate between alcohol consumption and cancer to my knowledge. The association is more with metabolic diseases because the liver is affected.

Alcohol is oxidised to acetaldehyde by alcohol dehydrogenase. Acetaldehyde may also, in turn affect the cells by DNA damage if it is not metabolized quickly to acetyl-CoA (perhaps in a manner similar to formaldehyde or by formation of Schiff's base with nucleotides). The other way by which alcohol is metabolised is through cytochrome-p450 (CYP2E1) which produces ROS (Hydrogen Peroxide), that may lead to carcinogenesis.

You might want to check this review.


Please explain what a gene isoform is in lay terms?

Gene isoforms are all the different RNAs that can be synthesised from a single gene. You may be referring to splice variants, which are systems of getting different mRNAs from the same sequence using different combinations of introns and exons.

(source: riken.jp)

Translating your wikipedia article:
Gene isoforms are the different RNA products obtainable from a gene that can vary on the place where the translation starts (protein synthesis), that have different sequences in the coding region (thus giving different proteins, sometimes with different functions) or by having different untranslated regions, UTR (the overhangs of the sequence that are not translated in the mRNA). This last difference, the UTR, normally gives rise to different stability within the cell as UTR secondary structures usually control the speed of degradation of an RNA.

Hope it helps


Are there any drawbacks to having immutable DNA during lifetime?

Semantic of the post
This question could arguably be better on-topic on WorldBuilding.SE. The difficulty with the kind of question that ask What if the world was different, it is unclear how different would it exactly so to understand what consequence to draw from this scenario. The other issue is of course that the answer cannot be drawn from empirical studies but only be inspired from current knowledge and make untestable predictions.
Because definitions of epigenetic vary and some of them might be extraordinary broad, I will assume that by mutation, you are referring to any change in the DNA sequence excluding epigenetic changes.
Related post
Does our DNA change during our lives? is a related post.
What do somatic mutations do?
Adaptive Immunity
For species having some form of adaptive immunity, somatic mutations are used for producing a large diversity of antibody than can be tested on the self before being released in the body searching for antigen to bind to. In absence of somatic mutations, the adaptive immunity is pretty much inexistent. This point is probably the most important and has been raised by @Polisetty in the comments.
Cancer
Somatic mutations cause cancers. More generally speaking, somatic mutations create genetic diversity within the body yielding to opportunity for selfish cells that could proliferate to the expense of the rest of the body. In absence of somatic mutations, there would be no (or at least much fewer) cancer. This will affect selection for increased lifespan.
Somatic mutations on genetic diversity
As a fraction of the mutations that are transmitted to the offspring occur before the separation between the somatic lines and the germline, the absence of any somatic mutation would result in a lower mutation rate. This would result in lower genetic diversity overall. It would also affect selection pressure that depend upon the mutation rate and may have other consequences that are hard to predict.
Also, and more importantly, many species undergo asexual reproduction such as budding in plants. In some species, the entire genetic diversity is caused only by somatic mutations. In absence of such mutation, there would be no evolution possible.
What mutations are inherited
If a parent has a mutation in the lineage giving rise to half the gametes, then this mutation will necessarily be passed to half of the offspring. For this reason, offspring tend to share new mutations even if their parent did not have them. Absence of somatic mutations will remove this effect, which I would predict would have little impact on anything!


Recommended reading to quickly get up to speed on infectious diseases

Since I didn't get an answer, I'll mention what I did.

My goal was to understand a particular disease well enough to talk intelligently about it while focusing mostly on the statistics. So learning Epidemiology from the ground up wouldn't have been practical in the 4-5 months I had.

I started with a high level patient-oriented book, C. diff in 30 Minutes. That gave me a general understanding of the disease. Then I began reading academic articles. Not only were these useful for citations in my paper, but it also helped expand my understanding. I would notice common terms that kept popping up. Gram-positive, rod shaped, anaerobic, endospore-forming is intimidating at first, but each of these modifiers can be googled individually to build an understanding.

Finally, it was necessary to know how much I needed to know. I began reading about the hypervirulent strain, ribotype 027 with its binary toxin yadda yadda. None of that was actually important for my paper because that level of detail wasn't in the data.

So while knowing the general landscape was important, knowing each and every detail, for my purposes, wasn't.


How can biologists rule out multiple early organisms that went through conjugation?

Because they would not use the same DNA codons. Codons are extremely conserved across life, with only minor variations, there is no reason this should be the case unless those codons are inherited from a common ancestor. This is contingent on what you mean by organism, prior to the incorporation of ribosomes it would be more possible.

If what you suggest had occurred it would drastically DECREASE the odds modern organism would share the same DNA.


Why are both glucagon and cortisol released in hypoglycemia?

Since the ability to utilize glucose for energy is necessary for life (look at the effect of hypoglycemia on brain function, for example), it makes sense that the regulation of serum glucose concentration would have a number of pathways, that is, redundancy helps to ensure continued proper function should one of the regulatory mechanisms fail.

Glucagon is considered the main physiological response to hypoglycemia; however, epinephrine, growth hormone, and cortisol - in that order - and very probably other factors yet to be named/elucidated also help to increase plasma glucose when it drops.

This kind of redundancy is very common. Cortisol, epinephrine and growth hormone all have other effects on tissue unrelated to glucose as well.

Glucose Counterregulatory Responses to Hypoglycemia


At least one group who have published on the effect of pressure on enzyme activity (Cho and Northrop) are not interested in it from a practical point of view, i.e. they are not subjecting enzymic reactions to pressures that they think they encounter naturally. Instead they are using the effects of pressure to test the kinetic and thermodynamic predictions of different models of enzyme catalysis. In particular they believe that pressure effects provide a means of testing the idea, first suggested by Linus Pauling, that an enzyme has a greater affinity for the transition state, rather than for the substrate.

This is explained in a paper on yeast alcohol dehydrogenase, but only the abstract is freely available. They claim to have evidence against Pauling’s idea, but I am not sure the extent to which this is generally accepted.


Are Restriction Enzymes obsolete with CRISPR?

No.

While CRISPR allows you cut a piece of DNA anywhere, you need to order a guide RNA to target your desired cut site. All standard plasmids still carry traditional restriction sites, and it's often convenient to use these. Using CRISPR as a restriction enzyme is probably more expensive and more complicated than using traditional restriction digest. Additionally, there are limitations about PAM sites with CRISPR. And you can always PCR a plasmid using whatever primers you want to produce a blunt end product that is "cut" where ever you want, and I'd bet the DNA oligos needed for PCR are cheaper than the guide RNA you need for CRISPR.


How can an enzyme favor even chained fatty acids?

The first experiment which showed that fatty acids are oxidized in C2-units has been done by Georg Franz Knoop and been published 1904 as "Der Abbau aromatischer Fettsäuren im Tierkörper.". The paper in reference 1 states:

  Georg Franz Knoop discovered fatty acid β-oxidation. In 1904, he
  published his classical experiments using odd and even chain ω-phenyl
  fatty acids such as ω-phenylvaleric acid and ω-phenylbutyric acid
  (Knoop 1904). Knoop fed these compounds to dogs and analysed their
  urine. In dogs that had been fed the odd chain fatty acids, he found
  hippuric acid (conjugate of benzoic acid and glycine), whereas, the
  dogs that had been fed even chain fatty acids excreted phenaceturic
  acid (conjugate of phenylacetic acid and glycine). From this he
  concluded that the metabolism of fatty acids proceeds by the
  successive removal of two carbon fragments. The remaining fatty chain
  had to contain a carboxylic acid. He postulated that oxidation took
  place on the β carbon atom, an oxidation unknown to organic chemistry.

If the fatty acid chain has an uneven number of carbon atoms, the resulting propionyl-CoA is modified into succinyl-CoA which is then used by different processes.

During the breakdown of the chain, Acetyl-CoA groups are released (at the end of each step), which can then be further metabolized by the body. Acetyl-CoA is fed into the Krebs cycle and then oxidized.

References:

A general introduction to the biochemistry of mitochondrial fatty
acid β-oxidation
Fatty Acid Oxidation


Why is the number of PCR cycles limited?

I would draw the line beyond 35, but thats a bit cosmetic.
The reasons are manyfold:

due to the exponential fashion of the amplification (ideally)
reagents are used up at some point
reagents degrade, this is especially true for the dNTPs
the activity of the enzyme, despite being heat-stable is declining
over time
beyond 35 cycles the exponential curve is flattening out (reasons see
above)
if you run the PCR for too long, you will get more and more
side-products (mostly primer dimers, but mis-aligned primers can also
make problems), this is more a problem for real-time PCR than for ones run on a gel

If you need a higher sensitivity with more cycles, you can use the technique called "nested PCR". There you do a first round with a primer pair specific for the region of interest and then do a second round with primers which are located slightly to the inside of the amplified DNA. This is done to avoid the amplification of unwanted contaminations. Since you do some 50-70 rounds of PCR amplification in total, this method is extremely sensitive (also to contaminations). See the image from the Wikipedia article for details:


A couple of half a minute? Anything under 5 minutes is a 90% chance of being safe if resuscitated. Drowning people don't make much noise because they are too distracted by the water. They only fill their lungs significantly after becoming unconscious.

simple description:
https://www.dedhamhealthfoundation.org/water/victim-recognition/stages-of-drowning/

complex description:
https://en.wikipedia.org/wiki/Drowning#Pathophysiology

The damages that occur are: lung injury, cardiac arrest, brain injury from oxygen deprivation.

The breathing pattern and physiology vary depending on hyperventilation, panic, physical exertion, fullness of the lungs at the time of submersion, so there is no simple answer to your query.

When they breathe significant amounts of water, it is because they have just lost consciousness and their body relaxes.

While they are is still conscious, they hold their breath for as long as they can, voluntarily / because they have breathed a sip of water and their epiglottis shuts and seals closed, by reflex.

There is a spasm called laryngospasm which occurs when the person is at the end of their breath and their body is trying to breath but their epiglottis is closed, that occurs at very low oxygen levels and a high oxygen debt because of the panic, so unconsciousness is only a few seconds away when the throat is convulsing, and it continues to convulse when they are unconscious and 90% of the time they breathe water and their heart continues beating.

I can't find how long it takes to have cardiac arrest after asphyxia or wet drowning. Probably it is not very well studied becuase it is so dangerous.

There is also the mammalian dive reflex, which occurs mostly in children who are suddenly immersed in freezing water. It can cause their metabolism and heart rate to go into slow motion, and stops circulation to their extremities, causing them to survive for more than 15-30 minutes.

This is a kayak trip heart rate with immersion in cold water.

From avalanche asphyxia, the heart can continue 15-20 minutes:
https://www.scancrit.com/2013/08/27/heart-rate-monitor-watches-avalanches/

There's a dutch man who lost his wife and then started diving in freezing water, and he can stay in freezing water for 30 minutes using conscious mammalian dive reflex.


What is the advantage of using starter cultures for growing bacteria?

Growth can be quite slow for some species under certain conditions when the concentration of cells is too low. Log-phase growth is powerful, and so one would like to keep cells in this state for the experiment at hand. Different genes are expressed then compared to a stationary phase.

In addition, you'd like your culture to out-compete a contaminant if there is one. That is more easily accomplished with a starter culture, which is then used to inoculate a larger culture for scale-up. Inoculating directing into the large-sized flask may allow your bacteria to enter a stationary phase, thus giving an opportunity for other species to out-compete your bacteria.


If you look in the results section of this paper on somatostatin-14, they explain that s-14 "is a fourteen residue peptide hormone where Cys$^3$ is disulfide bonded with Cys$^{14}$ to form a cyclic structure.

So your inclination is correct. The structure is cyclic and it is the cyclic structure which is responsible for the terminology. I don't know if there are exactly analogous structures with other than disulfide bonds but they would be cyclic for the same reason.

Another paper at page S1 talks briefly about the linear version of the same hormone, contrasting it with the cyclic form, again confirming that it is the structure that gives rise to the name, and not some other property.

It is the second reference that I think also answers the broader question: 'cyclic' is generic usage to describe a (simple or) complicated molecule containing a cyclic structure of joined atoms. Yet another paper (abstract) talks about cyclic vs. branched in a general way with respect to somatostatin and others:

"The aim of this contribution is to offer an unambiguous and general nomenclature system that enables researchers to represent all cyclic and branched homo- and hetero-detic peptides in a coherent manner in one-line text - as long as their as constituents can be represented in (three)-letter codes."

In this somewhat dated paper containing proposed IUPAC nomenclature for cyclic organic compounds, in cases in which there is a question whether a molecule is cyclic or not the prefix "cyclo-" enters the formal name. But in the title the origin of the issue is clear: "Nomenclature for cyclic organic compounds..." and again confirms that the usage is not based on the elements bonded but the ringlike structure.

There is a paper in which 'heterocyclic' (vs. 'carbocyclic') is used as a subclass of cyclic to refer to rings containing other than carbon. But the term cyclic applies to both.

Finally there is discussion of 'cyclic peptides' (wiki entry) generally which are classified 'according to the types of bonds that comprise the ring.' But they are cyclic because of the circular molecular structure notwithstanding considerable variation in the atoms (or multiplicity of bonds) comprising the ring.

Biochemistry has inherited much nomenclature from organic chemistry, and informal usage in textbook organic chemistry is that ringlike structures are called 'cyclic' whether they are comprised entirely of carbon or contain another element (typically N,O,S, etc.); for example 'cyclic ethers'--oxacyclopentane is a cyclic molecule containing oxygen.


Major effects on cells grown with 5% FBS supplemented media instead of 10% FBS?

If you were to run a flow-based viability assay (annexin V, live/dead fixable dyes, 7-AAD) or dual-fluorescence count (like acridine orange/propidium iodide, popular method as of late), you might find that more cells are undergoing apoptosis, or an increase in dead cells. I say this because trypan blue often overestimates viability. Your most pronounced effect should simply be a reduction in viable cells or a slower growth curve if you take those data points. Otherwise you'd need to run some test (fair example).

The problem being, these observations vary wildly based on what cell line you're using, lot-to-lot variability of the serum, and reagent handling. For example, the serum was heat-inactivated improperly, medium was degraded, bad lot of serum, and so forth. So take this as a generalization and a good reason to validate your serum lots.


Is fluoride toxic, and how worried should I be about it?

First of all: Yes, fluoride is toxic, but the toxicity depends largely on the form (soluble vs. unsoluble, which fluoride salt etc.) occurs. It also depends on the environment since insoluble salts which are subjected to strong acids can release fluorine ions.
The certain toxic dose for adults is 32-64mg/kg body weight, a 75kg adult needs to take up between 2,4 and 4,8 grams of fluoride ions (for sodium fluoride this would be between 5,3 and 10,6 gr of the salt). For children this is about 5mg/kg body weight.
For the water the added dose of fluorine is much lower, somewhere between 0,7 and 1.2 mg/l. Other sources of fluroride are food (especially sea food) and also black tea.

The toxicity of fluoride is mediated by different ways: First it forms an insoluble salt with calcium in the cells, effectively causing hypocalcemia. Calcium is an important second messenger in different signal transduction pathways as well as highly important for the functioning of nerve cells (which also explains why it is neurotoxic in the development of nerve and brain cells). It also causes the inhibition of a number of different enzymes as enolase (disturbs the glycolysis) but also phosphatases and katalase. For all of this have a look into the Wikipedia if you want to know more details.

About the paper: It is a review of published research articles which sums up the situation in this field. The paper mentions fluoride only twice: Once on the abstract and once in a table about newly identified developmental neurotoxins (table 2 to be precise). It references only one meta-analysis on this topic.

The cited meta-analysis ("Developmental fluoride neurotoxicity: a systematic review and meta-analysis") which did a statistical meta-analysis of published papers and their data. They find a significant relation between the fluoride content of the drinking water and the IQ of the children.
However this is not undisputed (to say it mildly), since while a finding can be statistically significant, it doesn't necessarily mean that there is clinical importance. The other important point which @Doctor Whom mentioned is that a correlation doesn't imply a causation. So even if there seems to be a correlation between two things, they are not necessarily connected (see the famous example of storchs and birth rates).

This paper ("Developmental fluoride neurotoxicity: clinical importance versus statistical significance.") is published as a comment on the original paper and claims exactly this. They say the the mean difference in IQ is about 7 points, which is not of clinical importance. Another paper critizes the relatively low quality of the original papers used for the study ("Fluoride and children's IQ.").

They also mention a low consensus about what is a high concentration of fluoride in the drinking water and also show the very wide variation of the fluoride concentration in the original studies. The highest concentrations mentioned are around 10mg/l which is about 10x the concentration used for adding fluoride to the water. Even if we take in account that children are more sensitive to fluoride and also need lower fluoride concentrations to cuse some developmental damages (below the fatal concentration) this would still add up to quite absurd amounts of water they have to drink.

Regarding your questions:

A developmental neurotoxin is a substance which interferes with developing neurons or nerve cells. It either inhibits their growth completely or at least impairs the cells.
Given on the articles I found (and cited above) I would say that fluoride is a developmental neurotoxin. Nevertheless it seems to me that it is not very strong in this context as the current studies are contradictory. Thinking about the amounts of fluoride present in water (even if the concentration is much higher than recommended) makes me doubt if this is really the causative agent.


What is the smallest oligocelluar organism?

The classic example, though I am sure there are others that are smaller, is the slime mold Dictyostelium discoideum:

It can have up to 100,000 cells and exists as both single cells and as a multicellular organism (emphasis mine):

  Dictyostelium amoebae grow as separate, independent cells but interact to form multicellular structures when challenged by adverse conditions such as starvation. Up to 100,000 cells signal each other by releasing the chemoattractant cAMP and aggregate together by chemotaxis to form a mound that is surrounded by an extracellular matrix. This mechanism for generating a multicellular organism differs radically from the early steps of metazoan embryogenesis. However, subsequent processes depend on cell-cell communication in both Dictyostelium and metazoans. Many of the underlying molecular and cellular processes appear to have arisen in primitive precursor cells and to have remained fundamentally unchanged throughout evolution. Basic processes of development such as differential cell sorting, pattern formation, stimulus-induced gene expression, and cell-type regulation are common to Dictyostelium and metazoans.


If all bacteria in human gut are dead, can they be there again?

So the question your essentially asking is "Do certain types of bacteria like a specific nutrient, and if so will they dissipate or die off if I do not acquire that nutrient?"

Let's give a specific example for comparison. Lactose intolerance is a prevalent disorder among many people and those who do have the intolerance, if aware, tend to steer clear from lactose containing foods. Some studies have been shown that correlate lactose consumption to amount of lactose-containing bacteria in the gut.

So I would say if your asking if you remove a nutrient from your diet will a particular bacteria suffer i.e die then yes. Although be aware that many bacteria are able to break down a variety of different nutrients, and in the case of a cupcake which is loaded with sugars, and fats, I would say a large majority of gut residing bacteria are able to use that as energy in one form or another.

Here's an article comparing lactose-tolerant, and lactose intolerant individuals, not chocolate, but a good start. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898492/


Retroviruses, like many other enveloped viruses, exit the cell by a process called budding. The virus uses the host machinery for producing transmembrane proteins to enrich areas of the host cell membrane in viral transmembrane proteins, and co-opts a host process for releasing vesicles.  You can see budding illustrated in the context of the life cycle of HIV in this figure from Murray Medical Microbiology.

The process has been studied in some detail in HIV and other retroviruses.


Did migratory birds' ancestors live in the places of migration?

Edited for a different consideration: Do birds migrate to and from zones defined only by ecological and climate choice, or do they evolve to migrate away to and from an ancestral home?

Later studies of migration searched for evolutionary definitions of bird migration as opposed to ecology/geography definitions which were the initial focus. Various theories of evolution and migration have been developed, although ice ages and climate change make the definition of a bird ancestral land vague.

If you search google for "sister taxa, migration, evolution" you will find a lot

A study for American Thrush species starts with previous research:

range expansion and speciation for the
evolution of long-distance migration. In brief,
resident, tropical species expand their ranges
into the seasonal subtropics. Further range
expansion into temperate areas due to competition
and other selective pressures creates a partially
migratory species. The partially migratory
birds continue to expand into higher latitudes,
where they breed successfully; migratory behavior
becomes fi xed (Stiles 1980).

It's results for the thrush are very complex, and you can see the map and the conclusions at the end, which state that:

The migratory species tree does not have a clear single ancestor.
The ancestor's range was probably very widespread, over 1000ds of
kilometers.
They migrated by stepping stone, rather than by diet
constraints of being frugivorous versus insectivorous.

http://www.sonoma.edu/users/g/girman/outlawetal2003.pdf
also
http://www.bioone.org/doi/abs/10.1642/0004-8038%282007%29124%5B410%3AASROMM%5D2.0.CO%3B2?journalCode=tauk

The data is erased in history, the migration routes and maps are very complex, the ancestral homeland shifts as forests and boreal ranges change latitude, so it's a balance in between the ability for birds to have fixed ancestral lands, given their great mobility, and the speed of their evolution. For the moment there are some theories on mechanisms and causes for selection by migratory advantage which are not general enough to apply to many clades of bird.

for precise and recent return to homeland:

Yes it's absolutely true, that many birds return to the exact same nest in Europe for example after wintering in Africa, and they also return to the same cliff/forest as where their parents were born, and some species vaguely follow the flocks very broad zones:

One study showed that most swallows returned to the same colony, with 44 per cent of pairs reoccupying the same nest. “This is remarkable given the length of a swallow’s return migration from its wintering grounds in South Africa,” says Rob Robinson, associate director of research at the BTO. Robinson has studied this iconic species’ unusually strong nest-faithfulness, a phenomenon called natal philopatry.

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


determining meaning of basic biological keywords about C. elegans

Have you discovered wormbase yet? It will become your new best friend. In worms gene names reflect the loss-of-function (lf) phenotype. Daf means "abnormal DAuer Formation," so daf-2 was the second daf gene identified (ref). The mutations are called alleles and each worm lab has their own allele designation. e was for England and in that lab's strain list the daf-2 allele was the 1,370th on their list. So daf-2(e1370) designation means that the strain carries a lf mutation in the daf-2 gene, and the specific allele is one that was isolated in Cambridge, UK. I believe that allele is temperature-sensitive (ts) dauer-constitutive.
So at 25⁰C 100% of the animals were dauers. That is when they harvested RNA. It is the entire transcriptome. It sounds like you may be familiar with modENCODE Data Warehouse. You can still ask questions about modENCODE datasets at help@modencode.org. While the modENCODE Data Coordination Center was mothballed at the end of the NIH funding period, there are a few people who still field queries like yours, to the Helpdesk. Also, moving forward the new ENCODE DCC has taken over curation of archival modENCODE metadata.


I would suggest looking up some basic sources on types of algae. For example, that source that I link to says this:

Algae vary considerably in size, shape, and growth form.
They can be:

Single celled
Many celled - either colonially or as filaments of cells; or
Elaborate plant bodies with differentiated cell types

In this case, I believe that Fucus would be in the third category ("elaborate plant bodies").
But note that these are informal categories, they don't really correspond to taxonomy or evolution or anything.


Is there any possibility that gender is determined by Temperature?

It is definitely more than science fiction. Many species have sex determination that depend upon the temperature.

As a rule of thumb, when it comes to sex, not much has been invented in fictions. The diversity of reproductive system is HUGE! I will not mention 1% of the existing complexity in sex systems. For simplicity, below I will limit my concepts and examples to big animals only. I won't talk about

double fertilization
cloning
parthenogenesis
dosage compensation
Mating types
Cases of multinucleated cells typically in fungi but not only
Asexual reproduction
Systems with more that two genders or with coexisting hermaphrodite along with a single other gender
Liability factor
Reaction norms for sex determination
How reproduction relate to all that
How dosage compensation relate to all that
How the concept of individual relate to all that
etc...

Sex Determination System: GSD vs ESD

There is a great diversity of sex determination system. The standard is to classify them in two

Environment Sec Determation (ESD)
Genetic Sec Determation (GSD)

Of course, the reality is more complex. In many species a mixture of both genetics and environment clues matter.

Within ESD species, there is quite a bit of variety. Some species use temperature (e.g. crocodiles, Nile tilapia, Australian skink lizard), others use social cues (e.g. clownfish, swordfish, boa constrictor).

Within GSD, there is also a great deal of diversity. By far not all species use the XY system used in mammals.

Related post

Do males of all sexual species have Y chromosomes?
Have there been any theories put forward as to the reasons behind Temperature-Dependant Sex Determination in reptiles?


Time taken for species to become endemic

From wikipedia > endemism:

  Endemism is the ecological state of a species being unique to a defined geographic location, such as an island, nation, country or other defined zone, or habitat type.

There is therefore no time component to it. If a species is found only in Canada, then it is endemic to Canada. If it is found only in your garden, then it is endemic to your garden. No matter the duration in which the species has been found in this specific location.

That being said, in conservation biology, it is common to oppose endemic species with invasive species. An invasive species

Wikipedia > invasive species

  An invasive species is a species that is not native to a specific location (an introduced species), and that has a tendency to spread to a degree believed to cause damage to the environment, human economy or human health

As the linked wikipedia page explains the concept of invasive species (or if you prefer the concept of non-endemism) is open to a lot of critics and is in no way well defined. There is no time limit under which we would stop considering an invasive species as invasive. It is rather the ecological impact of this species that will people to call it invasive or endemic based on purely subjective notions.


Does my brain have limited learning capacity or memory?

Short answer is yes, the brain has a limited capacity. It's a large but limited physical system with numerous but countable connection, it follows that it must have a limited capacity.

Learning wise, we usually say we learned something when we can recall it at will. I'm not sure I agree with that definition, but if this were the case, learning would be intimately related with memory capacity, so the answer would also have to be yes.

All this without taking into account energy consumption and metabolism which would impose also further limitations, e.g. I bet you that if you switch the activities around and start reading in the morning and try to work at night your work would suffer but your retention capability would improve (just a guess). Now, is all this relevant? I can't say, we (humans) might be working already at full capacity, in this case it would be relevant, or we could be very far away from this theoretical limit and all this is moot.

If that was really your question then you're done.

However, you seem to be preoccupied with a mismatch between the expectations of your own retrieval abilities after a particular "type" of activity and what you can actually remember.

I would be remiss in I didn't say that I agree with WYSIWYG's comment, I'm sure this is not the place for health advise. So with that in mind my 2c:

your expectations can be misaligned, that's always a possibility; your retrieval abilities can be impaired, which means that you learned fine but cannot recover it; or may favorite: you might just be tired! IANTTOAD


Cellular respiration — How is the water expelled?

Edited: I was wrong, the balance varies quite a bit by species. Reptiles and birds are far more water efficient than large mammals becasue they do not lose water through sweat or urine. There are animals that are metabolically water neutral, but humans are not one of them. In humans the water produced metabolically does far exceed the water used metabolically. I should have realized that reptile also produce less water. source 1source 2

In humans there are three main ways water is take in, drinking, injection (food), and a net metabolic production. There are four major losses, urine, sweat, respiration, and feces. so it is through one of these four methods.


Regarding the use of collagen supplements to help prevent or treat a tendinopathy:
A rather inconclusive quote from a 2016  systematic review {1}:

glucosamine and chondroitin sulphate, vitamin C, hydrolazed type 1 collagen, arginine alpha-keto-glutarate, bromelain, curcumin, boswellic acid, and methil-sulfonil-methane were considered […]. preclinical results are very encouraging, however they are not fully confirmed by clinical studies. There are few clinical papers on the use of nutraceuticals in tendon disorders, and their methodological quality is poor. Furthermore, in most of the studies more than one supplement was administered at the same time. This may bias the results, and the effect of each single component cannot be determined. Furthermore, the interactions between nutraceuticals and drugs, or other dietary supplements (especially at high doses) has not been evaluated, neither their effects on chronic diseases. For these reasons, it is not possible to draw any definitive recommendations on the use of nutraceutical supplementation in tendinopathies.

References:

{1} Federico Fusini, Salvatore Bisicchia, Carlo Bottegoni, Antonio Gigante,3 Fabio Zanchini, and Alberto Busilacchi. Nutraceutical supplement in the management of tendinopathies: a systematic review. Muscles Ligaments Tendons J. 2016 Jan-Mar; 6(1): 48–57. Published online 2016 May 19. doi:  [10.11138/mltj/2016.6.1.048] PMCID: PMC4915461. PMID: 27331031. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4915461/


Why do we define anaerobic respiration as not requiring oxygen, while utilization of the Krebs cycle and electron transport chain both require oxygen?

Because oxygen is not the majority of the energy.

Krebs cycle relies on sugars. Other processes use oxygen but can do without it or primarily use carbon fuels. So they are called anaerobic.


What does "Psychomodulatory" mean in the context of potentially psychoactive drugs?

To me, "psychomodulatory" would mean "eliciting a significant change (up or down) relative to baseline or compared to a control, placebo, or carrier," here specifically in CNS function.

This statement appears to refer to the results presented in section 3.8, Effect of euphol in the cannabinoid tetrad tests. Across a range of doses (3-100 mg/kg) and across four different assessments of CNS function: locomotor activity (rotarod), catalepsy (time to move off of a suspended ring), analgesia (tail flick in response to thermal stress), and body temperature (self explanatory). The results of these four are summarized in the figure below.

Basically the effects are not significantly different from each other between dosages or times. The lines sit more or less atop one another. Compare to this figure, where the differences are significant:


Reasons for a flower type to consume water faster than another?

Don't forget to consider the 'engineering' of the plant, as brought about by evolutionary history. Some plants will build fewer openings in their leaves ('stomata'); others use a strategy that allows them to only open these at night (see 'C4 photosynthesis') or CAM (Crassulacean Acid Metabolism) photosynthesis.


Why is saltatory conduction in myelinated axons faster than continuous conduction in unmyelinated axons?

Short Answer
Myelination acts as an electrical insulator and allows saltatory propagation.

By reducing membrane capacitance and increasing membrane resistance, myelination increases the velocity of signal (i.e., Action Potential) propagation.

If you want to see a really wonderfully simplified explanation, see this Quora post by Edward Claro Mader. Four great figures that Edward created show this phenomenon simply:
Decreased Membrane Capacitance:

Increased Membrane Resistance:

 Long Answer
So you're right: myelination speeds up electrical conduction. Unmyelinated axon conduction velocities range from about 0.5 - 10 m/s, while myelinated axons can conduct at velocities up to 150 m/s -- that's 10-30x faster!!
But why? ...
 Let's Look at Action Potentials & Signal Propagation:

You can get a background of this process in numerous places (e.g., here), so I will just mention this briefly:

When the neuron is at rest, ions are distributed so that the inside of the neuron cell is more negatively charged than the outside. This creates an electrical potential, called the resting membrane potential, across the cell membrane.

Sodium and potassium channels in the cell membrane control the flow of positively charged sodium (NA$^+$) and potassium (K$^+$) ions in/out of the cell to maintain this negative charge.

During depolarization, the cell membrane essentially becomes more permeable allowing NA$^+$ to enter the cell. This causes that section of axon to have a positive charge relative to the outside.

When this positive voltage is great enough (i.e., when an action potential is created), the influx triggers the same behavior in the neighboring section of the axon. Gradually, this positive charge on the inside of the cell moves down the length of the axon to the axon terminals.

 The Main Takeaway:
In this process, action potential generation occurs repeatedly along the length of the axon.
It's important to note two things about action potential propagation:

Each action potential takes time to occur.
The charge (i.e., voltage) that is created dissipates with $ \uparrow $ distance.

 Time for some Math & Physics:
In fact, we have equations to calculate both the time a voltage change takes to occur and how current flow decreases with distance.

You can read more about the mathematics behind this and passive membrane properties in general here and here.

Importantly, these equations rely on two constants: length and time.
The time constant, $\tau$, characterizes how rapidly current flow changes the membrane potential. $\tau$ is calculated as:
$$\tau = r_mc_m$$
where r$_m$ and c$_m$ are the resistance and capacitance, respectively, of the plasma membrane.

Resistance? Capacitance? Huh?...

Resistance = the measure of the difficulty to pass an electric current through a conductor.

Capacitance = the ability of a structure to store electrical charge.

A capacitor consists of two conducting regions separated by an insulator. A capacitor works by accumulating a charge on one of the conducting surfaces, which ultimately results in an accumulation of oppositely charged ions on the other side of the surface. In a cellular sense, increased capacitance requires a greater ion concentration difference across the membrane.

The values of r$_m$ and c$_m$ depend, in part, on the size of the neuron:

Larger cells have lower resistances and larger capacitances.

Importantly, however, is that these variables also rely on membrane structure.

c$_m$ (the capacitance of the membrane) decreases as you separate the positive and negative charges. This could be the result of additional cellular structures (e.g., sheaths of fat) separating intracellular and extracellular charges.

r$_m$ (the resistance of the membrane potential) is the inverse of the permeability of the membrane.

The higher the permeability, the lower the resistance.

Lower membrane resistance means you lose ions quicker and therefore signals travel less far

But why? This is where that length constant becomes important. The length constant, $\lambda$, can be simplified to:
$$ \lambda = \sqrt {\frac {r_m}{r_e + r_i} } $$
where, again r$_m$ represents the resistance of the membrane and r$_e$ and r$_i$ are the extracellular and intracellular resistances, respectively. (Note: r$_e$ and r$_i$ are typically very small).
Basically, if the membrane resistance r$_m$ is increased (perhaps due to lower  average "leakage" of current across the membrane) $\lambda$ becomes larger (i.e., the distance ions travel before "leaking" out of the cell increases), and the distance a voltage travels gets longer.
 Why am I telling you all of this??
How are the time constant and the space constant related to propagation velocity of action potentials?
The propagation velocity is directly proportional to the space constant and inversely proportional to the time constant. In summary:

The smaller the time constant, the more rapidly a depolarization will affect the adjacent region. If a depolarization more rapidly affects an adjacent region, it will bring the adjacent region to threshold sooner.

Therefore, the smaller the time constant, the more rapid will be the propagation velocity.

If the space constant is large, a potential change at one point would spread a greater distance along the axon and bring distance regions to threshold sooner.

Therefore, the greater the space constant, the more rapidly distant regions will be brought to threshold and the more rapid will be the propagation velocity.

Sooo....

If you increase the layer of cells around the membrane, you decrease the electric field imparted by extracellular ions, which allows intracellular ions to move more freely in the axon. In other words, you decrease the capacitance.

As a result, you have more cations available to depolarize other parts of the membrane.

If you decrease the permeability of the membrane (i.e., if you prevent ion pumps from moving ions in/out of the axon), you increase the resistance of the axon membrane, which allows for the voltage created in the action potential to travel farther before dissipating.

By allowing the voltage to spread farther before necessitating the generation of another action potential, you reduce the time it takes for signal propagation.

In other words, if you "block" ion pumps and decrease the concentration of anions near the axon membrane, you increase  membrane resistance (r$_m$) and decrease membrane capacitance (c$_m$), respectively. Together, this decreases the time of electronic conductance through the axon (and thus increase conduction velocity).
 Finally, to Myelin!
Myelin greatly speeds up action potential conduction because of exactly that reason: myelin acts as an electrical insulator!

Myelin sheath reduces membrane capacitance and increases membrane resistance in the inter-node intervals, thus allowing a fast, saltatory movement of action potentials from node to node.

Essentially, myelination of axons reduces the ability for electrical current to leak out of the axon. More specifically, myelin prevents ions from entering or leaving the axon along myelinated segments. As a result, a local current can flow passively along a greater distance of axon.

So instead of having to contantly generate new action potentials along each  segment of the axon, the ionic current from an action potential at one node of Ranvier provokes another action potential at the next node. This apparent "hopping" of the action potential from node to node is known as saltatory conduction.

 So Why not Just Myelinate the Entire Axon??
The length of axons' myelinated segments is important to the success of saltatory conduction. They should be as long as possible to maximize the speed of conduction, but not so long that the arriving signal is too weak to provoke an action potential at the next node of Ranvier. The nodes also can't be too frequent because, although adding a new node to the axon would increase its ability to generate sodium current, it would also increase the capacitance and thus diminish the effectiveness of other nearby nodes.

Sources:

Purves D, Augustine GJ, Fitzpatrick D, et al., eds. (2001). Neuroscience. 2nd edition. Sinauer Associates, Sunderland, MA.

The Brain: Understanding Neurobiology

Byrne, J.H. Chapter 3: Propagation of the Action Potential. Neuroscience Online. Univ. Texas.

Understanding the Passive Properties of a Simple Neuron

Quora

Wikipedia


Why is Psoriasis treated with Cortisone, when stress (which releases Cortisol) is known to aggravate the condition?

For treatment reasons cortisol is named Hydrocortisone (probably to avoid problems with the similar names) and this is often only referenced to as cortisone (although this is not correct). Cortisol (Hydrocortisone) is the active form, while cortison is not. See here for some more details.

Glucocorticoids (like Cortisol or Prednisolone) suppress acute inflammation and also have immuno modulative (downregulate) or suppressive function. Since the immune system causes the problems in Psoriasis it is downregulated to control the outcome of the disease.

First it sounds counterintuitive to use Glucocorticoids for the treatment of psoriasis as this hormone is released during stress (in this case to mobilize energy resources). However, there is a study which looked precisely at the cortisol levels in psoriasis patients and also recorded their stress levels.

What they found was interesting: First they could correlate the peaks in the stress levels with a psoriasis attack about four weeks later. Then they found that the Cortisol levels of the patients where significantly lower in stres situations than for healthy control persons. Additionally they found that patients which had permenant high stress levels also showed significantly lower permanent Cortisol levels. So here the stress seems to negatively influence the cortisol levels which then prepares the way for psoriasis attacks. Using high levels of topically administered Cortisol seems to reverse this effect.
You can find the study here:

How stress gets under the skin: cortisol and stress reactivity in
psoriasis.


Why is thymine rather than uracil used in DNA?

One major problem with using uracil as a base is that cytosine can be deaminated, which converts it into uracil. This is not a rare reaction; it happens around 100 times per cell, per day. This is no major problem when using thymine, as the cell can easily recognize that the uracil doesn't belong there and can repair it by substituting it by a cytosine again.

There is an enzyme, uracil DNA glycosylase, that does exactly that; it excises uracil bases from double-stranded DNA. It can safely do that as uracil is not supposed to be present in the DNA and has to be the result of a base modification.

Now, if we would use uracil in DNA it would not be so easy to decide how to repair that error. It would prevent the usage of this important repair pathway.

The inability to repair such damage doesn't matter for RNA as the mRNA is comparatively short-lived and any potential errors don't lead to any lasting damage. It matters a lot for DNA as the errors are continued through every replication. Now, this explains why there is an advantage to using thymine in DNA, it doesn't explain why RNA uses uracil. I'd guess it just evolved that way and there was no significant drawback that could be selected against, but there might be a better reason (more difficult biosynthesis of thymine, maybe?).

You'll find a bit more information on that in "Molecular Biology of the Cell" from Bruce Alberts et al. in the chapter about DNA repair (from page 267 on in the 4th edition).


Is it possible to grow a fertilized human egg entirely outside the woman's womb?

I believe what you're describing is referred to as ectogenesis which is essentially developing a fertilized egg inside an artificial womb until it’s able to survive outside the controlled environment. So is this possible outside of science fiction? To answer this we have to compare the stages of human reproduction and how close today's science and technology can come replicating/sustaining them.

We'll begin by dividing these stages into two groups: fertilization and development of embryo to fetus.

When it comes to answering the question of whether fertilization can be replicated in vitro or not, the answer is yes it can be done! In fact in vitro artificial fertilization (IVF) has been possible for several decades. In most cases when IVF is performed the egg is then placed inside the mother's uterus where it goes onto to develop into an embryo and then fetus. In regards to "ectogenesis" the IVF egg would be placed into an artificial womb.

In order to form a zygote (fertilized egg) to develop properly into a fetus it has to be an environment to meet it needs. In a female uterus all these needs are met but replicating them might be difficult. An artificial womb would have to be able to provide nutrients, oxygen, and channels for the development process of a fetus as well as system to expel (birth) the fetus once its development is complete. So can today's technology and science do all this? In theory yes, if resources and time where dedicated (and red tape cut) it would be possible to develop a fertilized egg in an artificial environment within the foreseeable future. There have been multiple experiment where artificial wombs were implanted with fertilized eggs and began to grow but were stopped due to legality.

I encourage you to read the following Wikipedia and motherboard articles regarding artificial wombs and ectogenesis.

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

http://motherboard.vice.com/read/artificial-wombs-are-coming-and-the-controversys-already-here

*Note there is a lot of biology I did not mention regarding zygote to fetus development which is the biggest question/obstacle that ectogenesis might face


Why do the two hemispheres of the brain control the opposite sides of the body?

Just to get the ball rolling here.  This particular aspect of brain evolution is very old. The cross wiring of the hemispheres of the brain seems to be as old as the right and left hemispheres itself.  It predates lizards - i.e. hundreds of millions of years ago. It  possibly predates right/left dominance and the organ asymmetry which puts the heart on the left side of the body.

Digging back deeper, we can see that worms have bilateral brain structure, but as noted in the comments below, the nervous systems do not cross.  I would guess that this means that the phenomenon appears sometime before lizards - putting the development having been done by the early Carboniferous period when the first animals came to the land and the first reptiles appears, which is the perhaps 350 million years ago.

Echinoderms (like starfish) are 'missing links' in bilateral symmetry as their larval stage has bilateral symmetry even though the adult has radial symmetry.  Such wiring may be so embedded in the way most animal body plans develop that it hasn't changed in evolutionary history. If that is related to other animals trait, it could be a billion years ago. Some argue this is not the case.

One might guess that the cross over of neurons in brain control is good for integrating the signals from both sides of the organism. There are quite a few theories.