When analyzing whether selection favors an allele that allocates indiscriminately, should the initial frequency of the allele be considered?

I have not read the paper but here is my guess and a hint

  Is it a typo?

Yes, I think so

  In a situation in which altruism is not directed toward any particular individual(s) but is rather allocated to the whole population, doesn't r depend upon the frequency of the allele that is engaging in the altruism?

Yes

  f it is a new mutation and there is no other allele in the population to receive the benefit, then r=0. If the allele has gained fixation, r=1 and selection is much more likely to favor the altruism.

If the allele that is causing altruism has reached fixation, then there is no more selection as there is no genetic variance in the population.


'Big ideas' behind constrained selective breeding (optimization)

I believe that you are talking about "multidimensional selection".
E.g. you are selecting on not one trait (yield) only but more than one (yield+some other trait). There's quite a bit of work done on this in crop science for example.
See e.g.

here
here
here

Figure 3 from the last talks about this in terms of evolution by reproductive isolation, which is pretty much the same thing except it's natural rather than artificial selection.

The most important thing practically is to try to measure the correlations of the traits in question. If they are positively correlated or uncorrelated, it shouldn't be too hard. If they are negatively correlated then you might have some difficulties due to constraints on the kinds of phenotypes that can exist.
For a recent technical treatment with good references, see here.


Identification for a bird in the middle of the tree

Yes, Lesser whitethroat indeed. Grey head with contrasting white throat and brown body, small bill (the similar Orphean warbler has a much bigger bill).


Does mixing alcoholic drinks really make you more drunk?

There are some very general answers to your question.

Definitely, there is a lot of magical thinking. We as humans are very prone to anecdotical evidence and extrapolations from incomplete data, even more so when we are drunk.
As an interesting "proof" is the fact that the German counterpart of the saying "beer after wine and you'll feel fine, wine after beer will make you feel queer" is "Wein nach Bier, gönn' ich Dir, Bier nach Wein, lass es sein" -- which means the exactly opposite of the English saying (beer after wine is bad, wine after beer is fine).

Many kinds of alcohol contain unwelcome additional substances, for example fusel alcohols. Definitely, "mixing" broadens the range of these additions.

Mixing can lead to a misperception about the actual amount of alcohol that was taken in. Many people who would not drink a vodka and drive have no problem driving after a half a liter of beer (which contains same amount of alcohol two shots of vodka).


Can a non-response to a vaccine be tested?

You can test for antibody titers (and also connected memory) for the persons who got the vaccine and then decide, if these antibody levels are protective or not. Problem with this method is, that it is not clear, what levels are protective. There is still no experience with it for SARS-CoV-2, this is routinely done for other diseases.
According to clinicaltrials.gov, the study design is a placebo controlled trial triple blinded (Participant, Care Provider, Investigator) which enables the direct comparision of the vaccine arm with the placebo arm. Here you analyze the difference between these arms. If the vaccine delivers a sufficient protection, less (or ideally no) people in the vaccine arm get sick - which is exactly what was observed.
A last possibility would be to challenge people, who received the test vaccine with the virus and see, if they develop the disease. However, this approach is highly unethical since you possibly infect a large number of people with a potentially deadly virus, when the vaccine does not work. I doubt that a researcher who wants to do this will get clearance for these experiments by the internal review boards involved in these trials.
This is done in earlier stages in animal experiments, to challenge the immune response.


What kind of a microscope do I need to see cell organelles?

groups of cells

A normal light microscope. 4x-20x magnification

  individual cell

Lo resolution: Light microscope with 40x magnification.

High resolution: Confocal microscope with 40-100x magnification.

  cell organelles

Low resolution: Confocal microscope with >=60x magnification.
Note: some organelles are easier to visualize while others are difficult. With confocal you can manage to see almost all of them with low resolution i.e you will be able to detect their location and distribution but wont be able view their fine structure.

To view the structure of organelles you would definitely need an Electron Microscope.

  Is there a difference between digital and non-digital microscopes for that purpose?

If you are not too much into the optics of it then I guess it wont matter. I prefer if it has an analog mode along with a digital mode. Image acquisition is anyways digital.

Popular models: Leica, Zeiss and Olympus are popular brands. You select the model as per your requirements.


Can potassium ions depolarise neuron membranes?

Yes, this is a very basic neuroscience question, something that would probably come up in the first week of a neurophysiology class or unit.
The polarization of the membrane at rest is due to cells being primarily permeable to potassium at rest, and due to a concentration difference of potassium inside vs. outside the membrane. Inside, potassium is high, outside potassium is low.
Therefore, there is a concentration gradient such that if a cell were at 0 mV, potassium would be flowing out of the cell. There is a membrane voltage where this net flow would stop. We refer to this as the "reversal potential" or "equilibrium potential" for an ion. For potassium in a typical cell, this tends to be around -90mV. The larger the ratio of concentrations in versus out, the larger the potential. You can calculate this potential with the Nernst equation if you know the concentrations (image from Wikipedia):

From this equation you can see that the reversal potential is negative for a positive ion if [outside] is small compared to [inside]. By applying higher potassium outside than usual, the ratio of [outside]/[inside] gets closer to 1, so the reversal potential for potassium is closer to 0mV, and typical neurons that are mainly permeable to potassium at rest will depolarize.


How does non-homologous end joining (NHEJ) work?

Non-homologous end joining indeed induces errors in the affected sequence. But you have to keep in mind, that NHEJ is an emergency repair mechanism which involves a "repair or die" chance. If the chromosomal break is not repaired it is not unlikely that the cell will get into apoptosis, or, even worse, develops into a cancer cell. Introducing small errors is a relatively small price compared to this, although this can still disrupt genes or regulatory sequences. For the mechanism have a look onto the figure (from the first reference):

For further reading have a look onto the Wikipedia article on NHEJ and/or the following references:

The mechanism of human nonhomologous DNA end joining.
The mechanism of double-strand DNA break repair by the nonhomologous
DNA end-joining pathway.


It is protection against rapid warming of the cambium layer. A lot of far northern timber has light colored bark which reflects sunlight. The rapid heating from very cold after sunrise can actually damage or even split the bark of dark colored species. This is called sunscalding.


Why plants (eg. parsley) can keep vitamin C despite all the sun?

UV light promotes the photo-oxidation of ascorbic acid (AsA) to dehydroascorbic acid (DHA).

DHA can be reduced to AsA by a specific dehydrogenase using reduced glutathione as reductant. I'm pretty sure that all cells are able to carry out this recycling of ascorbate.

Interestingly, in plants it appears that ascorbate acts as an electron donor to photosystem II (which is equivalent to it being oxidised).


Why are enzyme-catalysed reactions slower at lower substrate concentration?

Alan Boyd's answer covers the mechanistic aspects quite well, but there is another aspect he didn't quite touch on - what's going on at the molecular level. To understand this, you need to think about the actual conditions of the reaction: unless it's taking place inside a cell, which straight biochemical reactions of the kind you're talking about almost never are, then the enzyme, substrate, and product are all floating around at a certain concentration. The enzymatic reaction is proceeding nicely, and as the substrate binding pocket is freed as product dissociates from the enzyme and diffuses away, allowing another substrate molecule to take its place and the next reaction to occur. This is the situation at your 2 mmol [substrate] level. At 50 mmol, the concentration of substrate is much higher, and so even though the actual catalytic portion of the enzymatic reaction is taking place at essentially the same speed, the rate of substrate diffusing into the active pocket is somewhat higher because the local concentration of substrate is higher, allowing for an apparently slightly faster reaction rate.


My answer is messy and incomplete! I very welcome editing!

As soon as an individual is killed, on might as well eat the dead, but the act of killing might not be for the purpose of eating. We might even say that eating a dead might not only be for the purpose of getting energy and matter but only to clean the living place. And killing might appear in many circumstances. The best way to consider such issue is certainly by using the quite fundamental model of kin selection theory. It fits as much to species that gain energy by eating the dead or not. The difference imply just a minor change in the payoff matrix.

The decision of one (the actor) to kill (and eat) another individual (the recipient) depends on:

the relatedness of the actor to the recipient (note a relatedness is not necessarily symmetric)
The competition this recipient causes on the actor
The cost (energy cost, risk of being injured or killed) of killing

Many species (ants, wolves) might kill or injured individuals of the same species, when for example there is competition for reaching a status in the hierarchy.

I think that the definition of k-selected species is not very accurate. First because there are limit cases. But also because r and k can relate to the function that describes the population growth of a species or might describe the amount of energy the parents spend into one offspring which is not necessarily the same thing. If we think of the parental care, we can think of the lions. When a male win the right to access to the females of another male, he will kill the babies that might be potential competitors to his progeny (because they take energy from the females or because females are not fertile before having lost their babies).

Killing its own offsprings is certainly not less common in k-selected species. You might think it is such a big cost to kill one of its own offspring when one has few offspring but what is important is to think in percentage. Killing 50% of the progeny has the same cost of an r-selected species than for a k-selected species.

If one has a probability of 10% to be able to raise its offspring to adult age. But this probability raised to more than 20% if it accepts to kill an offspring to save energy for the next offspring, then it wins by doing so. THen we might ask: "so would one make an offspring if it intends to kill it?"

Well it does not necessarily intend to kill it. It might need to decide late in the season whether or not it has better to kill its own offspring.

Then, maybe offspring might be used as a reserve of energy and matter for its siblings or for its parents.


How does UV light damage the DNA when the chromosomes are deep inside the cell?

UV Rays kill the cells by damaging the DNA. UV lights do not disrupt the cell membrane. If a cell is exposed to UV light, it creates THYMINE dimers (bond). Thymine dimers are the actual disruption in the kinks of DNA. UV exposure to skin is proportional to the cell damage.

P53 is a gene product which takes care of fixing cell damage. However it has a tolerance. If the damage is less, P53 sends damage repair machinery. If it's non-fixable, then P53 directs the cell to programmed death.

More UV exposure, more thymine dimers causing more cells to die (cell death). If the damage is not extensive, then that may cause cancerous cells (Result of cell damage).


Why doesn’t p53 cause the repair of cellular DNA that has been altered experimentally?

I am no expert in this area, and this answer is only based on a reading of the Wikipedia article on p53, which you should perhaps have read carefully. I welcome edits or correction by persons more knowledgeable than me on this topic.

First, although the Wikipedia article neglects to mention it, you can forget about bacteria as the protein is only found in eukaryotes.

Second, one needs to consider what exactly p53 does in relation to protection of DNA from mutation, how it is activated to do this, and hence whether this would occur in the circumstances of the introduction of mutated DNA into a eukaryotic genome.

From the article it appears that “It (p53) can activate DNA repair proteins when DNA has sustained damage”, and that “p53 becomes activated in response to… stressors, including… DNA damage (induced by either UV, IR, or chemical agents such as hydrogen peroxide)…”

The manipulation of animal DNA will be performed outside of the target organism, and the modified DNA re-introduced into the genome by one of several mechanisms that are unlikely to evoke the stress signals that are evoked by agents that damage DNA ‘naturally’. Hence there is no reason to expect the activation and action of p53 in response to this type of experiment.


It might depend on the signal that the seed uses to end dormancy. Some seeds require 'vernalisation', that is a prolonged period of low temperatures, for them to germinate successfully.  If they don't have the cold period, they don't germinate because they 'think' that they haven't had winter yet.

Dormancy can also depend on the conditions that the parent plant lived under, so it is quite possible that if two plants were grown in different environments, their seeds would have differences in dormancy. This study looked at that effect in the 'model plant' Arabidopsis thaliana:
Donohue K., Dorn L., Griffith C., Kim E., Aguilera A., Polisetty C. R., Schmitt J. Environmental and genetic influences on the germination of Arabidopsis thaliana in the field. Evolution. 2005;596(1):740–757.

This paper gives a good review of Seed Dormancy and Germination in Arabidopsis from a few years ago:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3243337/#i1543-8120-70-1-1-b60


Why would the citrulline content of the watermelon be so high?

According to molecular botanists and plant physiologists, watermelon is the only plant that is known to contain significant amounts of citrulline. Interestingly, it appears that the reason for this tremendous enrichment in citrulline stems from the environment in which wild watermelons naturally thrived hundreds of years ago prior to the development of agriculture.

According to botanists, drought is one of the most severe stresses to which a plant can be exposed. Drought generates a high level of free radicals and oxidative stress, in part because plants maintain their photosynthetic machinery even in the face of severe drought. A number of investigators have shown that different plants have unique molecular mechanisms/systems to allow them to tolerate such harsh conditions and oxidative stress.

Wild watermelon plants inhabit the Kalahari Desert in Botswana, where the annual rainfall is less than 2 cm. Despite the minimal rainfall, the watermelon (a xerophyte) can tolerate the extreme conditions well with an exceedingly high drought tolerance. Surprisingly, this tolerance to intense drought conditions by watermelon plants even persists despite a sub-optimally developed root system. In the case of the watermelon, citrulline is overproduced in the leaves (and apparently the rest of the plant) and citrulline acts as the major hydroxy radical scavenger that allows wild watermelon to tolerate the drought-induced oxidative stress. From this same source (Annals of Botany - link below), there are also other proteins that may also be involved in these mechanisms as well. Even though the citrulline content is predominately used in the leaves to buffer oxidative stress, it appears that it secondarily accumulates in the melon itself.

Note: The image below is from Annals of Botany paper in the links below - it is OPEN ACCESS, which is why I posted the picture and included the reference link. You can clearly see the before and after pictures of drought and how the watermelon leaves appear minimally changed, unlike the radish and cucumber leaves.

See below for some interesting Papers about citrulline, watermelon, and mechanisms of drought-resistance:

Ann Bot. 2002 Jun;89 Spec No:825-32.
Citrulline and DRIP-1 protein (ArgE homologue) in drought tolerance of wild watermelon.

FEBS Lett. 2001 Nov 23;508(3):438-42.
Citrulline, a novel compatible solute in drought-tolerant wild watermelon leaves, is an efficient hydroxyl radical scavenger.


Do antagonist-receptor complexes get absorbed into the cell?

When a neurotransmitter, like serotonin, binds to it's specific receptor, the ligand-receptor complex is not phagocytosed.  Picture the human cell membrane and think of the serotonin receptor like a long piece of rope that has been wound up, but is embedded inside the cell membrane forever.  After the serotonin binds, the structure of the receptor changes, causing lots of steps to start (like a domino effect) where molecules are released from the inner aspect of the receptor, thus carrying the message into the nucleus.


Why are abiogenesis and evolution considered unrelated?

I wouldn't go so far as to say that they are entirely unrelated -- our understanding of selective processes can certainly inform our study of the origin of life -- but I would say that they are quite different projects.

One important reason is that evolutionary biologists can use phylogenetic information to reconstruct much of the history of life. For example, genetic sequencing techniques allowed us to definitively work out the evolutionary relationships among humans, chimps, and gorillas. But this approach can only allow us to back as far as the last universal common ancestor (LUCA). LUCA was presumably a DNA-based (uni-)cellular lifeform, given that these characteristcs are shared across the entire tree of life. So we have no phylogenetic information that we can leverage to reconstruct what happened to get us from a soup of organic molecules to LUCA.

Another reason is that evolutionary biology focuses on what happens to a population in which we have variation, heritability, and selection. Early in the origin of life, a structured system of heredity would not yet have arisen and so we would not see natural selection occurring in the form that we usually study it -- though there could be interesting selective dynamics in such a system.


Is there such thing as "meters per calorie" for living organisms?

Halsey & White (2012) Comparative energetics of mammalian locomotion: Humans are not different. Journal of Human Evolution 63:718–722

This paper presents a comparison of the metabolic cost of walking and running in humans, Australopithecus and other mammals.  They use a parameter NCOT (net cost of transport), whose units are ml O2 consumed m-1. The inverse of this parameter would be related to your metres per calorie.

The authors quote an NCOT of 12.77 ml O2 m-1 for a walking human. Using a value of 4 kcal g-1 for glucose, I calculate that this NCOT is equivalent to 14.6 m kcal-1.

Here I found an energy consumption value of 5.8 kcal min-1 (for a 73 kg man) walking at 6.4 km h-1, which translates to 18.5 m kcal-1.

Incidentally, according to the authors of the paper:

  The predicted net cost of transport (NCOT, ml O2 m−1) of mammals is related to mass (M, kg) according to 0.54M0.70.


People say the cardiac cycle depends on blood pressure? How so?

There are two levels to take your question at.  The first is simpler but I'm not sure if it is what you are looking for:

If you imagine the heart and all the blood vessels in your body as a closed plumbing system with no leaks (not entirely accurate) then when the heart contracts and squeezes the blood from the ventricles the total surface area the blood is pushing against has decreased - there is more blood in a smaller space.  This means that the pressure on the arteries from the blood has to increase when the heart contracts - in systole blood pressure is much higher than in diastole.

The second level is a little more in depth:

Cardiac output (a measure of how much blood is being pumped around the body to the organs where it is needed) is defined as the product of stroke volume and heart rate.

$$CO = SV \times HR$$

Heart rate is the number of times the heart beats per unit time
Stroke volume is the amount of blood that is pumped out of the heart in one beat. It is this that is related to blood pressure.

The relation of stroke volume to blood pressure is defined by Starling's Law.  This states that the more blood that is in the heart, the more its walls are stretched.  The more the walls are stretched, the harder the heart contracts in response.  This increases blood pressure as again more blood is displaced from the heart.


Does any molecule other than DNA have a double-helical structure?

A few examples:

Starch
A polymer of glucose that can form a double helix and functions primarily as energy storage in plants.

[image source]

f-Actin
Filamentous actin forms a helical structure with two strands of polymerized g-actin. This is a structural component of the cytoskeleton.

[image source]

Coiled Coil
Protein motif with a helical structure formed by two (or more) α-helices. Coiled coils are found in a diverse range of proteins from structural proteins like keratin to transcription factors like c-Fos.

[image source]

Gramicidin
A peptide-based antibiotic that has been shown to form membrane spanning double helices.

[image source]


Thus, there is a significant selection pressure for humans to develop resistance but no (or almost no) pressure for toxoplasmosis to counter human resistance.

Well, I think in this case "Significant" isn't qualified. Significant selective pressure can come in many forms, but as you mention about 30% of humans are infected with Toxopolasma, and the vast majority remain capable and functional. Remember that selective pressure applies to the ability to take advantage of resources and reproduce. People with toxoplasmosis are almost always capable of surviving and reproducing, so I doubt the pressure is all that much.

There is also significant incentive for Toxoplasma to develop the ability to adapt to humans, as it would open up a whole new resource for them to take advantage of. How fast the parasite is capable of adapting, or even if it's possible to eventually include humans in their life cycle, is something that would take some studying.

Our immune systems, in turn, try to kill the parasite regardless of whether we're being taken advantage of or not. You might be interested in reading up on the Red Queen Hypothesis - a theory that delineates how the immune system is at constant war with its environment and potential new threats.

As for your last question...

  ... why are so many people infected?

That's easy. :-)

Cats have become a popular pet, and most of the time the parasite doesn't significantly affect us. If either of those changes, you'll see a change in infection rates.


What is the difference between a fixed substitution and a single nucleotide polymorphism (SNP)?

If you look into a certain population, you will find mutations (for example SNPs) in some ratio with the wild-type allele. When a mutation reaches fixation, it will be the only allele, reaching 100% penetrance in this population. See here for more information.

In the context given I would interpret it in the way that a total of 464 SNPs were found, 430 of these were in fixation (so can only be discovered when comparing them to another population) and 34 SNPs which haven't reached fixation and thus cannot be found in all members of the population.


Does a generator potential pass along a nerve the same way an action potential does?

Generator potentials (GP) are meant to generate action potentials (AP). An action potential results, whenever the level of depolarisation at a particular place crosses a threshold. This "place" is usually the beginning of an axon of a typical receptor, since it is equipped with all the channels required to begin and propagate an action potential. The purpose of the receptor architecture, then, is to make the threshold go off in a naturally meaningful situation.

There are two possible ways this is done. Say the neuron is transmitting information about the location of a stimulus. Then the "naturally meaningful threshold" would be some spatial cutoff, a minimum area that needs to be stimulated for the action potential to go off. Then, the receptor would have several GP-producing dendrites spread out, each generator potential being summed at the meeting place of the dendrites, which happens to be the cell body and the beginning place of the axon. So the individual generator potential in each dendrite will contribute to the sum, which will be summated and the cellular decision-making process (or a crude example of it) be affected as this summation.

Another way is temporal summation, something which has, for example only one GP-producing dendrite and the axon. Then, for the summated potential at the cell body to cross the threshold, the stimulus must stay, or be summated across, for some time-cutoff. GPs have some decay time, before which if another GP reaches there, it adds up. This would be meaningful in things like the presence or absence of a touch, the cutoff preventing against minor fluctuations.

This said, the situation in the eye in much much more complex. There are several layers of neurons and each neuron performs a lot of different functions and has a specialised architecture for it. The Rods and Cones actually produce hyperpolarizations and not depolarisations (theoretically, both are propagated in the same way, but hyperpolarisations themselves do not initiate AP).

To complicate further, most receptor systems alter the frequency of AP and thus have some basal frequency, this modulation also being important for encoding the message.

An image of GP:


Why is lower case used in front of a capitalized acronym (e.g. rDNA)?

It's just a stylistic approach because "DNA" or "RNA" is an abbreviation by itself that has become a whole noun. Those terms clearly separate the modifier from the overall DNA/RNA. It makes it easier to read. Terms like DNA and RNA are almost always known just by those acronyms, whereas something like mRNA is known both as "messenger RNA" and "'m' RNA" but almost never as "messenger ribonucleic acid."


How do sporozoites travel into the human host when the mosquito is sucking blood?

Nice question!  Basically, the mosquito does not only suck; it also injects some saliva into the host with its saliva glands.  From National Geographic:

  The mosquito starts salivating as soon as it probes the [host]’s skin, releasing substances that prevent blood vessels from constricting, stop blood from clotting, and prevent inflammation. Sometimes, Choumet could see the saliva as small bubbles that hung around the tips of the mouthparts. And even after the mosquito stops feeding, pockets of saliva linger in the lower layers of the skin.

And from cdc.gov:

  After 10-18 days, the parasites are found (as "sporozoites") in the mosquito's salivary glands. When the Anopheles mosquito takes a blood meal on another human, the sporozoites are injected with the mosquito's saliva and start another human infection when they parasitize the liver cells.

The probiscus is actually equipped to inject saliva as well as to suck blood.  And once the saliva has entered the victim, it can spread to the whole body since the blood is constantly moving.  From mosquitnoband.com:

  Mosquitoes also have special hematophagous arthropod saliva in their proboscis. Hematophagous arthropod saliva is a scientific way of saying “spit from a blood-sucking creature with an exoskeleton.” This specific type of saliva has chemicals and proteins in it that prevents blood from clotting. So what do mosquitoes do with their hematophagous arthropod saliva? They inject it into their victim before they start sucking its blood to prevent any clotting while they slurp.

Hope this helps!


Is Sda a protein, or is it a protein domain of DnaA?

Short answer

Wikipedia has unnecessarily made an already confusing situation much worse. Sda is its own protein, it is regulated by DnaA, and it prevents sporulation.

Full answer

I don't think your misunderstanding is based on the meaning of 'domain' - the definition you give sounds quite reasonable - but rather the use of the term domain with respect to Sda and the naming of Sda itself, which I agree is quite confusing and made much worse by Wikipedia in this case.

Sda is a protein that inhibits KinA activity (Burkholder et al., 2001) and is a completely separate protein from DnaA. I don't see where you jumped from your notes to the idea that Sda is a domain of DnaA except for from Wikipedia: I don't know why Wikipedia thinks Sda is a protein domain, it is a protein. It is a very small protein, so perhaps it would be appropriate to think of it all as one domain, but there is not a single result for "Sda protein domain" on Google Scholar - no one else is using this terminology. A full Google search only returns a few (~150) results, most of which are direct copies/translations from Wikipedia, or Wikipedia is a direct copy of them. Wikipedia can be useful, but if it starts to cause you confusion, don't assume it is correct.

The phrasing "KinA is bound and destabilised by Sda, a DnaA target" means that Sda binds KinA and destabilizes it, and notes that Sda is a target of DnaA; since DnaA is a transcription factor, you can infer that this means that DnaA controls expression of Sda in some way.

In biology a checkpoint just refers to a place that a process can be halted/arrested, often in reference to the cell cycle. Sda is considered a checkpoint because when Sda is expressed, it prevents cells from sporulating by indirectly preventing activation of Spo0A (Burkholder et al., 2001).

Another source of confusion is that the name "suppressor of dnaA" on Wikipedia is WRONG, but further, molecular biologists sometimes have an impenetrable way of naming things, owing to the complexity of control of gene expression and the circuitous way that new proteins are identified and understood.

The correct name for sda is "suppressor of dnaA1". dnaA1 is NOT DnaA - dnaA1 is a MUTANT ALLELE of DnaA that results in cells that are completely unable to sporulate. But! sda is also NOT Sda: sda is a MUTANT ALLELE that produces non-functional Sda (the protein).

I'll quote from the title of the table in Burkholder et al:

  sda Mutations Suppress the Sporulation Defect of dnaA1 Mutants

Or, stated again, in dnaA1 mutants, there is a defect in DnaA which prevents sporulation. The researchers searched for mutations that would reverse this effect. They found one, and named it sda, because it reverses (suppresses) the effect of the mutation they were studying. The dnaA1 mutant's effects on sporulation seem to be caused by an increased expression of Sda, which is why the sda mutant reverses the effect.

References

Burkholder, W. F., Kurtser, I., & Grossman, A. D. (2001). Replication initiation proteins regulate a developmental checkpoint in Bacillus subtilis. Cell, 104(2), 269-279.


Functional role of voltage-gated potassium channels

The meaning of reversal potential

Ion channels do not themselves have reversal potentials except for via a weighted average of the ions that they conduct. The reversal potential for a given ion is given by the Nernst equation and besides physical constants is a function only of the relative concentrations of ions inside and outside the cell.

The equilibrium potential of the whole cell is given by the Goldman equation, which is similar to the Nernst equation but covers any number of ions. Note that you can also calculate a "reversal potential" for a channel using the Goldman equation by considering all the ions that a given channel will conduct.

The reason that a cell's equilibrium potential at rest is not equal to the potassium reversal potential is because cells are not permeable only to potassium at rest; although potassium dominates, there is some conductance to other ions, which depolarizes the cell slightly.

There is no way for a potassium-selective channel to have a reversal potential any different from the potassium reversal potential, unless it were to be permeable to other ions as well.

What would happen if there were no potassium channels?

If there were no potassium channels at all, cells would rest near 0 mV, give or take a few mV. The "leak" channels that allow cells to rest at a negative potential are primarily potassium channels. However, it seems like your question is mostly directed towards voltage-gated potassium channels.

What would happen if there were no voltage-gated potassium channels?

As you suggest, cells would repolarize much more slowly. However, your question still has inaccuracies.

1) This repolarization would not be from sodium diffusing away, it would be from potassium leaving the cell through leak channels.

2) The sodium-potassium ATPase is not directly responsible for the membrane potential or for repolarization in an action potential. Ion concentrations change very little during an action potential. The thing that changes is the permeability to different ions. The sodium-potassium ATPase is important, however, for maintaining the relative inside concentrations of sodium and potassium ions over the long term.

In addition, as you also suggest, there would be no afterhyperpolarization.

Is there a purpose to the afterhyperpolarization? Is it just unavoidable?

There is somewhat of a purpose. Although the afterhyperpolarization isn't strictly necessary to get action potentials to fire, there are some hyperpolarization-activated channels in some cells, and in all cells the hyperpolarization facilitates the removal of the inactivation block of sodium channels. In general words, it serves as a bit of a 'reset signal' beyond mere repolarization.

However, the afterhyperpolarization is also pretty much unavoidable without a very fine-tuned engineering of the repolarization process (you would need to rapidly close potassium channels as they approached rest, which would also slow down the return to rest).

Overall, this material would be well-covered in an introductory neuroscience textbook. My personal recommendation is Purves:

Purves, D., Augustine, G. J., Fitzpatrick, D., Hall, W. C., LaMantia, A. S., McNamara, J. O., & White, L. E. (2014). Neuroscience, 2008. De Boeck, Sinauer, Sunderland, Mass.

(any other edition is fine, too, and there a lot of other good alternatives as well)


Burns' "To a mouse" - what species of mouse?

It could be Wood Mouse(Apodemus sylvaticus).

Courtesy : redbubble.com


This appears to be some species of beetle (order Coleoptera) in the Bostrichidae family.

Commonly called auger beetles, false powderpost beetles, or horned powderpost beetles.

 Xylopsocus capucinus

Identification to species can be difficult, but fortunately for you Sittichaya et al (2009) created an illustrated key for IDing species associated with South Asia.

Based on their key and visual characteristics of your specimen, my guess is that your specimen is Xylopsocus capucinus

 Source: Sittichaya et al 2009 . a. lateral view; b. elytral declivity; c. intercoxal process of the 1st abdominal ventrite; d. dorsal view.

Description: 3-5.5 mm long; 1.4-1.7 mm wide. Shape is cylindrical and similar in general appearance to other common species of the family Bostrichidae.
Distribution: throughout South and Southeast Asia from India to the Indonesian archipelago.
Hosts: apparently polyphagous attacking almost any woody plant in suitable condition.
Phenology: adults emerge mainly
between May and November.

Like most false powderpost beetles, the head cannot be seen from above as it is downwardly directed and hidden by the thorax:

 Source: UFL IAFS

Sources:

Sittichaya, W., Beaver, R., & Ngampongsai, A. (2009). An illustrated key to powder post beetles (Coleoptera, Bostrichidae) associated with rubberwood in Thailand, with new records and a checklist of species found in Southern Thailand. ZooKeys, 26, 33.
Woodruff RE, Gerberg EJ, Spilman TJ (2005). A False Powder-post Beetle, Xylopsocus capucinus (Fabricius)
(Insecta: Coleoptera: Bostrichidae). University of Florida, IFAS Extension Publication No. EENY-179.
Institute of Food and Agricultural Sciences, University of Florida, 4 pp


I don't believe so.  I have never come across a eukaryote that does not have introns although there are some genes that do not contain introns.  Some eukaryotes like ciliates actually contain other non-intronic intergenetic regions that seem to be nonfunctional.  These are called Internally Existed Sequences and are removed from the germ-line active micronucleus before going to form the transcriptionally active micronucleus.  Interestingly, introns are also present in these organisms and are present in both the micro and macronucleus.  These introns are spliced out in textbook fashion.  I believe one of the organisms where introns was discovered was in Tetrahymena thermophila with the intron in the rDNA sequence.


Well remember that an mRNA, the RNA that is destined for the ribosome, has already been processed by the time it gets there. This is done by the splicing machinery, among other things (capping enzymes, for example). But the splicing machinery isn't smart in itself. Rather, the gene has the elements, just like it does to select the RNA Pol it needs, to direct the sort of modification the RNA needs to obtain. The image below depicts two types of RNA transcribed by RNA Pol II and how the processing elements let the modification machinery know how to handle them:

Source


Mechanical cause of loss of consciousness

Mechanical force can compress neurons and cause action potentials as you probably experienced in the form of hitting the funny bone. Strong enough acceleration of the brain tissue may be causing massive excitation of neurons as indicated by animal EEG study. It suggests that the loss of consciousness is due to generalized epileptic seizure. However, it is not fully agreed upon: quoting wikipedia entry on Concussion:

  It is not known whether the brain in concussion is structurally
  damaged or whether there is mainly a loss of function with only
  physiological changes.[14][needs update] Cellular damage has
  reportedly been found in concussed brains, but it may have been due to
  artifacts from the studies.[15] It is now thought that structural and
  neuropsychiatric factors may both be responsible for the effects of
  concussion.[16]

And following quote is from this

  The brief loss of consciousness that characterizes concussion appears
  to be the result of rotational forces exerted at the junction of the
  upper midbrain and thalamus that cause transient disruption of the
  functioning of the reticular neurons that maintain alertness.
  (Allan H. Ropper, M.D., and Kenneth C. Gorson, M.D.; N Engl J Med 2007; 356:166-172 January 11, 2007)


What is the difference between tonic and phasic firing?

Tonic firing typically occurs without presynaptic input and can be viewed at as background activity. Tonic activity is often characterized by a steady action potential firing at a constant frequency. Note that not all neurons may have tonic activity at rest. It may serve as keeping a steady background level of a certain neurotransmitter or it can serve as a mechanism where both an inhibition or increase in presynaptic input can be transmitted. When a neuron is silent at rest, only an increase in presynaptic activity can be transmitted postsynaptically.

In contrast, phasic firing occurs after a neuron is activated due to presynaptic activity and it incurs activity on top of any background activity a neuron may have. It is typically restricted to one, a few, or a short burst of action potentials, whereafter the activity quickly returns to the resting state.

Reference
Tsai et al., Science (2017); 324: 1080-4


What animal's lower eye lid moves to upper one when closing eyes?

Actaully there are quite a few animals which actually moves there lower eyelids:

Most of the birds
Reptiles(Except Snake)
Amphibians


Where can I find free authoritative images of different species of Lagomorphs?

Wikipedia is good for this,
The licence is what you want, and many people will have checked the animal ID.
look up the two pika species, and the rest are under
http://en.wikipedia.org/wiki/Leporidae


Thank you for asking such a well-thought out question, I really enjoyed how hard this made me think about the concept. I think there might be an issue here that's quite common to biology, in my experience- poor definition of terminologies.
I think the core question can be summed up by your comment:

I thought dominance was only related to which phenotype will show. If fitnesses of $A_{11}$ and $A_{22}$ are equal, doesn't it mean just that $A_{11}$ and $A_{22}$ have the same chance at surviving?

In my thinking, the definition of dominant could mean two things:

The expression of a particular characteristic
The fitness associated with the expression of a characteristic

Of course, the second definition depends entirely on the first- if the phenotype of the heterozygote ($A_{12}$) is the same as the homozygote ($A_{11}$ or $A_{22}$), then their fitness must be the same- evolution acts on phenotypes, not genotypes.
Let me break this down using Gillespie's tables. For a given value of $s$ (between 0 and 1), we can imagine the following scenarios for the value of $h$:

$h$
Phenotype
$A_1A_2$ fitness
Dominance scenario

h=0
$A_1A_2$ phenotype = $A_1A_1$ phenotype
$1-s\times 0 = 1 = A_1A_1 fitness$
$A_1$ is dominant allele

h=1
$A_1A_2$ phenotype = $A_2A_2$ phenotype
$1-s\times 1 = 1 - s = A_2A_2 fitness$
$A_2$ is dominant allele

This is assuming the phenotype for $A_1A_2$ is the same as the phenotype of the homozygote, in each scenario. It may be possible that the phenotypes are different, but the fitness is the same- what we are actually measuring with $h$ and $s$ are fitness, not phenotypes. But if the phenotypes are the same, the fitnesses must also be the same- natural selection works on phenotypes, not genotypes.
Where the break between fitness and phenotype becomes complete is when $h$ is a value other than 0 or 1 (not complete dominance).

$h$
Dominance Type
Scenario

0<h<1
Incomplete dominance
The heterozygote ($A_1A_2$) more fit than $A_2A_2$ and less fit than $A_1A_1$

h<0
Overdominance
The heterozygote ($A_1A_2$) more fit than homozygotes ($A_1A_1$ and $A_2A_2$)

h>1
Underdominance
The heterozygote ($A_1A_2$) less fit than  homozygotes ($A_1A_1$ and $A_2A_2$)

In each of these cases, the phenotype of the heterozygote is something different than either of the homozygotes (hence the term incomplete dominance). What the value $h$ is measuring here is not the difference in phenotypes, it's the effect it has on fitness- which might be different in different contexts.
Let's think about the classic example of overdominance, sickle cell disease. In terms of fitness, individuals with one copy of the sickle cell allele have the sickle cell trait. The sickle cell trait offers resistance to malaria, and therefore higher fitness in regions with endemic malaria. An individual with two copies of the sickle cell allele are less fit because they have sickle cell disease. An individual with no copies of the sickle cell allele is less fit because they don't have resistance to malaria infection.
But this measure of dominance, where we define dominance as the fitness associated with a the expression of a characteristic, is context-dependent- individuals with the sickle cell trait are prone to other diseases, and in the absence of endemic malaria it might be they have lower fitness than an individual with no copies of the sickle cell allele ($0<h<1$).
If we think about dominance as simply the expression of a characteristic, we would actually describe the sickle cell heterozygote as co-dominant- when you look at the blood of individuals with sickle cell trait (heterozygotes), they have a mix of normal-shaped red blood cells and sickle-shaped red blood cells.
So to conclude:

Dominance sometimes refers to the expression of a trait in relation to an allele, and sometimes refers to the fitness associated with the expression of a trait in relation to an allele.
Differences in fitness imply differences in phenotype (because natural selection acts on phenotypes, not genotypes)
Differences in phenotype do not necessarily imply differences in fitness

I wrote also some notes on the following, but as they're not directly relevant to the question (but might be useful for Googlers later on) I will put them here below the cut:
Table of relative fitness measures with dominance coefficient $h$ and selection coefficient $s$

Genotype
$A_1A_1$
$A_1A_2$
$A_2A2$

Relative fitness
$1$
$1-hs$
$1-s$

The choice of alleles assigned to $A_1$ and $A_2$ are arbitrary- in reality these are As, Ts, Cs, and Gs. By convention the first allele is the dominant one, but if you're not sure which is dominant before you test it may be the second!
Similarly, by convention we assume the individual with $A_2A_2$ is not more fit than individual with $A_1A_1$ (in other words, $0<s<1$). But you might have it backwards!


Can a plant be programmed to produce any arbitrary object?

It could not fit in a comment...

1) Any material have some physical limitations and living tissue are not exceptions. A plant cannot resist to very high pressure without changing shape for example. Outside of these problems of material sciences I think the major considerations are technical…

2) It is possible to influence the shape of a plant by changing its DNA code, changing its physical and chemical environment (micro or macro environment) or by injecting some substance. Today we might be able to influence the number of branching of certain plants species for example. But we are terribly far from having enough knowledge in biology (in genotype-phenotype map, in biochemical pathway) in order to transform a dandelion into a shopping mall! Even we had already described all chemical pathway linking genes to phenotypic traits, it is immensely more complex to think of which kind of DNA sequence might transform a plant into something that is so different.

I don't know if anyone has ever created a totally synthetic (and not copied from already existing sequences) DNA sequence and could predict the impact it would have on the organism phenotype. Some people were able to create a totally artificial self replicating RNA though.

Note: Some people play with the properties of the DNA molecule in order to create various tissues. This might interest you as well.

One can highly improve this answer by giving some results of studies on synthetic life.


Is there a minimum load below which an infectious agent will not cause disease?

It depends on the pathogen, delivery method, environment, etc. In most cases, a single pathogen is not enough to cause disease -- it may need many millions or billions -- but there are some cases where it does seem that a single pathogen can consistently cause infection. For example

  The minimum infectious dose of ASFV in liquid was 100 [i.e 1] 50% tissue culture infectious dose (TCID50), compared with 104 TCID50 in feed. The median infectious dose was 101.0 TCID50 for liquid and 106.8 TCID50 for feed.

--Infectious Dose of African Swine Fever Virus When Consumed Naturally in Liquid or Feed

If you're asking specifically about smallpox, I don't think anyone has done the experiment (the natural and most susceptible host being humans, I think you'd have some trouble finding volunteers to find to lethal dose). A single virus of the related ectromelia (mouse pox) virus can cause death in particularly susceptible mouse strains:

  The intranasal lethal mousepox model employing the A/Ncr mouse strain is used to evaluate anti-orthopoxvirus therapies. These infections mimic large droplet transmission and result in 100% mortality within 7-10 days with as little as 1 PFU [plaque-forming unit] of ectromelia virus.

--Mousepox in the C57BL/6 strain provides an improved model for evaluating anti-poxvirus therapies

As a side note, the notion of what a "single virus" actually is, is more fuzzy than you might think, but that's a more complicated question; to a rough approximation a single TCID50 or PFU can be considered to be a single virus.


Length of dispersal flight of European spruce bark beetle?

The number of days may still be unknown, and it is probably a large variation when they find a suitable host tree. The "pioneer males" might use "random-walks", when they try several trees before they chose the right one. Its also a large difference between endemic and epidemic periods regarding dispersals.

Anyhow, the flight distance of I.t. has been shown to be more than 8 km (see Botterweg, 1982), but during outbreaks when it can be pheromone sources everywhere most of them may disperse less than 500 m and maybe even less than 100 m. See:

Kautz. 2011. Quantifying spatio-temporal dispersion of bark beetle infestations in epidemic and non-epidemic conditions.

Whichmann and Ravn. 2001. The spread of Ips typographus (L.) (Coleoptera, Scolytidae) attacks following heavy windthrow in Denmark, analysed using GIS

and as mentioned above, the dissertation by Kärvemo and articles within.

I hope this helps.

cheers

Simon


Searching for raphide purification I came up with a paper where they isolate these crystals from kiwi fruit:

Konno, K., Inoue, T. A., & Nakamura, M. (2014). Synergistic defensive function of raphides and protease through the needle effect. PloS one, 9(3).

Does that help?

Note, however, that while according to this paper these large crystals can be kept in suspension that isn't the same as a solution ...


Fingerprints are called epidermal ridges in Biology. These are formed between the 3rd and 4th month of the fetus. The epidermal layer looses its strength, becomes like a cloth from a piece-board and falls on the underlying layer of skin cells, the dermal papillae. Now, you must realize that not all tissues are as smooth as the skin for evolutionary reasons. This tissue, although a part of the skin, is irregular and some its cells get little more swelled up. After falling, the epidermis begins to harden up and thus takes its shape.
This phenomenon has probably evolved from providing friction for traction and increase in surface area for sweat to come out.
Read more at:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1013024/


The best cyanobacterial pool is the World Ocean.

No man, no amount of venture capital investment, no board of directors, no CEO, no CFO, no CSO, etc. can ever create, on the Earth, an equivalent to the World Ocean.


Are Italians genetically separated from other Europeans?

I'm afraid that the "genetic island" idea is almost certainly wrong because

The wikipedia page offers no evidence for this claim:

  Following scientific research carried out by Dutch geneticists, Italy has proven to be one of the last two remaining genetic islands across Europe (along with Finland), this due to the presence of the Alpine mountain chain that, over the centuries, has prevented large migration flows aimed at colonizing the Italian lands.[citation needed]

Remember that any random idiot person can edit a wikipedia page. If there is no supporting reference for a claim you find in wikipedia, you should treat it as suspect.
As you point out, the Alps only block entry on the north of Italy. Italy, however, is a pretty large peninsula, completely open to the sea along its entire length. For example, here is a map of Greek and Phoenician colonies circa 530bc (source):

As you can see, significant parts of the coast of what today is Italy were colonized by Greeks and Phoenicians. There were many subsequent waves of migration and/or invasion by various tribes such as

The Lombards (image source):

The Visigoths who sacked Rome in AD410
The Ostrogoths whose kingdom in its prime contained most of modern Italy

The many Jewish communities in Italy that go as far back as the Roman era.

An article by Brisighelli et al. (which is actually quoted at the very top of the Wikipedia page you linked to) mentions that (emphasis mine):

  A total of 583 individuals were sampled from across the Italian Peninsula, from ten distant (if homogeneous by language) ethnic communities — and from two linguistic isolates (Ladins, Grecani Salentini). All samples were

  [...]

  Italy shows patterns of molecular variation mirroring other European countries, although some heterogeneity exists based on different analysis and molecular markers. From North to South, Italy shows clinal patterns that were most likely modulated during Neolithic times.

  [...]

  Before the Roman conquest, ancient Italy was characterized only by the presence of Indo-European populations living in the Italian Peninsula since the second millennium BC, corresponding to the period between the Iron Age and Romanization. During all this period there were also increasing contacts with the Phoenician and Greek colonists: the former being largely present on the coasts of Sardinia and western Sicily and the latter in Southern Italy.

  [...]

  At the beginning of the first millennium BC the following native tribes could be distinguished on the Italian territory: the Ligures, on the coast that bears their name, in the northern Apennine valleys, part of the pre-alpine valleys and the western Po Valley; the Sicani, in the interior of Sicily; and the Itali, in present-day Calabria (from whom comes the name ‘Italy’, which was to be extended to all the territory of the peninsula). Besides the already mentioned Terramare tribe, on the southern edge of the Po Valley, and the Villanovans, probably from Eastern Europe who settled throughout Central Italy, there were also the Umbrians to the east of the upper basin of the Tiber. The Veneti, who occupied the territory that still bears their name, originally came from Illyria as did the Messapii (now modern Salento or South Apulia) and Iapyges, who settled in present-day Puglia (Apulia) 5. Many other populations of Central-Southern Italy were created by the mixing of local and foreign elements dating back to the previous millennium; it is the case of the Sabines and Latini who settled in Lazio together with Falisci, Aequi, Volsci, Hernici and Ausones. The interior of Abruzzo was dominated by the Vestini, Paeligni and Marsi, while the central Adriatic coast was populated by Picentes, Marrucini and Frentani. The Apennine area of Molise and Basilicata was peopled by the Samnites and Lucanians. In Calabria and Sicily there were also the Bruttii and Siculi.

  [...]

  Molecular indices indicated that most of the Italian samples show diversity values that are comparable to other European populations. However, some differences were shown to exist, especially in isolated Ladin populations.

References

Brisighelli F, Álvarez-Iglesias V, Fondevila M, Blanco-Verea A, Carracedo Á, et al. (2012) Uniparental Markers of Contemporary Italian Population Reveals Details on Its Pre-Roman Heritage. PLoS ONE 7(12): e50794. doi:10.1371/journal.pone.0050794


Probably you used bad keywords. It is called cytokine (or interleukin) network what you are looking for. There are several articles in the topic.

For example:

Cytokine patterns during dengue shock syndrome
Multiplex cytokine profile from dengue patients: MIP-1beta and IFN-gamma as predictive factors for severity

You can find here more:

https://scholar.google.com/scholar?q=cytokine+networking+in+dengue


Do reproductive organs function before puberty?

No, they are not functional before puberty.

For males:

  Most males begin puberty between the ages of 9 and 14, but commonly puberty will begin around 12 years old. When the human body reaches a certain weight (which differs among individuals), the hypothalamus releases gonadotropin-releasing hormone. This hormone signals the pituitary gland to release the two hormones that begin the onset of puberty: leutinizing hormone and follicle-stimulating hormone.7 In males, these hormones stimulate activity in the testes, which start to produce the male sex hormone testosterone and begin spermatogenesis. Spermatogenesis is the process of sperm production.

source (warning: contains NSFW drawings and images)


Brown marmorated stink bug (Halyomorpha halys):

Source: Brown marmorated stink bug (wikipedia)


Do the pH and other ions affect the hydrolysis of ATP

Stability of ATP is largely due to Mg2+. ATP in cell is actually Mg2ATP2-
The Mg ions stability the negative charges on the phosphates. pH is also important of course, but Mg is key, hence you see Mg2+ all the time in biochemical reactions where ATP is involved.


That is the work of a leaf miner. A leaf miner is the larval stage of an insect that feeds on the inside layer of leaves. Notice how the galleries (tunnels) start small and then get larger as the larva matures? Most leaf miners are moth larvae (Lepidoptera)
https://en.wikipedia.org/wiki/Leaf_miner


There follows an attempt to answer my own question, which I think is important to consider in the general context of postings on SE Biology concerning uracil and thymine in DNA and RNA synthesis.

There seems to be little misincorporation because of the low concentrations of dUTP in cells.

Any small amount of misincorporation can be handled by the DNA repair system that exists in cells.

I base statement 1 on the work of Grogan et al., published in Biochemistry 50, 618–627 (2011). They showed that in both mouse and human cell lines that the normal concentration of dUTP (and dUMP) was low. I assume that this must reflect cellular activities of dUTPase and thymidylate synthase being sufficiently high to remove dUTP and dUMP, respectively as they are formed. When thymidylate synthase activity was inhibited by anticancer drugs, these nucleotides built up, as expected.
In support of Statement 2 I refer to a separate earlier study in fission yeast by Seiple et al. in Nucleic Acids Research 34, 140–151 (2006). They used the drug, 5-fluorouracil, to inhibit thymidylate synthase and found that it caused misincorporation of uracil into DNA with concommitant cell damage. The role of the DNA repair system in mitigating this damage was shown using a mutant in the Ung1 gene, which encodes DNA glycosylase — here the cell toxicity was much higher.
Although there are some inconsistancies between the different systems used, and difficulties of interpretation.  I think that they provide general support for the two postulates. It would be useful if it were possible to locate kinetic data on the relevant enzymes to test my assumptions regarding the reason for the low dUTP concentration.


This is in between a comment and an answer...

Notes

reptiles can have several definitions. Some of them causing birds to be a reptile.
You probably meant "evolved" instead of "developed".
Thermoregulation is performed by a set of different mechanisms and it is plausible that your question would be considered as too broad. Note however that I am NOT a physiologist and might overestimate the scope of the question.

Similitudes between birds and mammals

From wikipedia (here)

  In cold environments, birds and mammals employ the following adaptations and strategies to minimize heat loss:

  Using small smooth muscles (arrector pili in mammals), which are attached to feather or hair shafts; this distorts the surface of the skin making feather/hair shaft stand erect (called goose bumps or pimples) which slows the movement of air across the skin and minimizes heat loss.
  Increasing body size to more easily maintain core body temperature (warm-blooded animals in cold climates tend to be larger than similar species in warmer climates (see Bergmann's Rule))
  Having the ability to store energy as fat for metabolism
  Have shortened extremities
  Have countercurrent blood flow in extremities - this is where the warm arterial blood travelling to the limb passes the cooler venous blood from the limb and heat is exchanged warming the venous blood and cooling the arterial (e.g., Arctic wolf[3] or penguins[4][5])

  In warm environments, birds and mammals employ the following adaptations and strategies to maximize heat loss:

  Behavioural adaptations like living in burrows during the day and being nocturnal

  Evaporative cooling by perspiration and panting
  Storing fat reserves in one place (e.g., camel's hump) to avoid its insulating effect
  Elongated, often vascularized extremities to conduct body heat to the air


a) stronger aggressive behaviour only during egg laying
c) stronger aggression when egg is first laid than during nest building
d) greater aggression during hatching eggs than during nest building

These all occur after the stage which determines fitness. Egg laying (a and c) and Egg hatching (d) occur after the male has won the right to mate.

b) stronger aggressive behaviour during nest building rather than
during hatching of eggs

Assuming the behavior increases mating success and fitness, the answer is B because this is the only strategy that attracts more females and gets rid of rival males before it is too late (i.e. before the female mates). This is also assuming that the female can/will only mate once.
In chronological order the answers run "B,C/A,D" (C & A are really one and the same in my eyes). Mating occurs between B and C.


Which virus capsids consist of only one type of capsid protein?

Interestingly, the fact that viruses might be made up of repeating subunits was a hypothesis by the famous Watson and Crick in 1956.

A useful resource for this is the Viral Zone website maintained at by the ExPASy bioinformatics system. It contains an easily browsable and human interpretable list of viral families and their characteristics. In particular, you can "browse by virion" which will show you different structural classifications of viruses; make sure to look at all the different genetic classes of viruses (single-strand RNA, double-strand RNA, DNA, etc).

From my preliminary investigation, it appears that many capsids are composed of only a single subunit; in addition to TMV, some other examples I found are the totiviridae family of viruses which infect single-celled eukaryotes such as Giardia lamblia, the human-infecting astroviridae and calciviridae families, and (as far as I can tell) the Heptatitis B virus. It also appears that Dengue virus has a single capsid protein.

As for the tertiary structure of capsid subunits, you might find this review of interest. Basically, due to symmetries in the shape of icosahedra (or helices or other geometric shapes adopted by capsids), you can argue that the structure of subunits in certain symmetrical parts of the capsid has to be the same (because they are copies of the same protein and, by positional symmetry, they have to be experiencing the same forces). When there are asymmetries in the structure of the icosahedron, then it is often hypothesized that there exists a state of "quasi-equivalence;" that is, the deviation from symmetry is small enough that the tertiary structure of each subunit is not affected very much. The review goes into these points in much greater detail.


With every round of PCR, your sample doubles (ideally) and you are right when using $2^n$ for calculating the amount of DNA produced.

The formula would basically be like this:

$$X_{n} = X_0 2^n \\[1em] n=\log_2(X_n/X_0)$$

Just substitute the values of $X_0$ and $X_n$ — 10ng and 1000ng. The answer would be ~6.64 cycles.

The 500ng case is easier to imagine. The amount is doubled between 1µg and 500ng. So it is just one cycle of PCR.

If this was your answer then you are right. If book says otherwise then it is wrong or you could have read the question wrong.


What are the visual, behavioral similarities and differences between Yellow Fever Mosquito (Aedes aegypti) and the Tiger Mosquito (Aedes albopictus)?

For the best way to tell them apart, see this guide: http://www.cdc.gov/dengue/resources/30Jan2012/comparisondenguevectors.pdf

Specifically, it seems that the silver pattern on the torso is different (lyre-shaped for Yellow Fever Mosquito, more linear for Asian Tiger Mosquito).  Location is probably also an important determinant.


The brain is indeed stacked with blood vessels, as shown in a 3D model in Fig. 1.

Fig. 1. 3D-printed model of blood vaculature. Source: Biobots.

The blood supply on the surface of a live brain is readily seen during a craniotomy (Fig. 2.)

Fig. 2. Surface of the brain. Source: The Sterile Eye.

When freshly prepared, the interior of the brain appears pink, indicative of the presence of blood (Fig. 3):

Fig. 3. Coronal sections of a non-fixated brain. Source: Documenting Reality.

Mostly, images of the brain are taken after fixation of the brain. The fixation process includes removal of the blood in the brain and the fixative pales the color of the tissue markedly. Fixation results in the more familiar pale-appearing pictures of the brain as shown in Fig. 4.

Fig. 4. Coronal section through a fixated brain. Source: Wikimedia.

Also note that the blood supply mainly targets the areas where the cell bodies are located, i.e., the gray matter. The white matter is pretty much devoid of blood supply and mainly consists of heavily myelinated, fatty tissue supporting axonal fiber tracts (Fig. 5).

Fig. 5. Arterial innervation of the brain. Source: Human Physiology Academy.


Do some colors trigger more neural activity in human brain?

The paper from Stoughton & Conways (2008), where the linked Design Shack webpage refers to, explains that in the visual nucleus in the brainstem (LGN) as well as in the primary visual cortex, most of the color-selective neurons are selectively responsive to colors in the red-cyan axis (Fig. 1).

Fig. 1. RGB color space. source: Commodore 128 forum

This indeed means that these colors evoke more brain activity in these regions of the brain.

Note that a perception curve mentioned on the linked D'Source webpage is nonsense terminology


The phenomenon you describe, where the same result comes about in more than one time/location via evolution, is called "convergent evolution." It is when the same character, or trait, evolve independently of one another. One example is the wing, it has evolved (at least) several times independently, in bats, birds, and insects. Parallels can also be drawn with other traits like dispersion methods of seeds, or the evolution of fins in fish, dolphins, and whales. Here is a classic paper by Ernest Williams from 1972 which describes one of the earliest examples given of ecomorphs, the anolis lizard, also talked about on this site.

This is from a good article on the new scientist website that would be worth reading:

  "Evolutionary convergence occurs at every level, from proteins to
  societies. An unusual antibody once thought to be unique to camels has
  a close equivalent in sharks, for instance, while naked mole rats form
  social colonies like those of ants and bees.

  "What this means is that if we could wind the clock back and let life
  evolve all over again, life might take very different paths but still
  produce organisms that, in some ways, resemble the organisms alive
  today.

  "There would almost certainly be streamlined swimmers in the oceans and
  winged creatures in the skies. In fact, some argue that the evolution
  of intelligence is also virtually inevitable, though intelligent
  organisms could be very different from us."

The answer to your question is yes, with enough time and the same selection effects we would not be surprised if there was a similar pair of independently evolved characters. However, selection acts on random mutations which is not a directed process, therefore for the same characters to evolve you would need mutations to occur that had similar effects. This is why given enough time we can see the same responses. Despite the non-random effect of selection, we could consider evolution to be a stochastic process, it only arrives at the same converged point by chance. This is because selection (the main driver of evolution) acts on randomly generated genetic variation thus the direction of the evolutionary trajectory is random.

  "..often used to represent the evolution of some random value, or
  system, over time. This is the probabilistic counterpart to a
  deterministic process (or deterministic system). Instead of describing
  a process which can only evolve in one way (as in the case, for
  example, of solutions of an ordinary differential equation), in a
  stochastic or random process there is some indeterminacy: even if the
  initial condition (or starting point) is known, there are several
  (often infinitely many) directions in which the process may evolve." -
  wikipedia entry on Stochastic Processes

Following the quote above it may seem that evolution is a directed process, i.e. selection is aiming for a specific target. It is not, selection can only weed out the least fit genotypes and increase the frequency of the better ones, selection has no goal or pre-existing aim. Thus, when discussing stochasticity in evolutionary terms it is perhaps better to use evolutionary trajectories, to describe the randomly created paths they move along, instead of "directions."

As an example of convergent evolution we could use the peppered moth and a little imagination because this is purely a hypothetical illustration I am making up on the spot.

The peppered moth is famous for once being a white moth that turned dark during the industrial revolution, when towns and cities grew and pollution killed the light coloured lichens that helped the light morph hide. This meant, rather suddenly by evolutionary time-scales, the white morph of the moth was not very well camouflaged against the dark bark of the trees. This created a positive selection for darker morphs, as such, alleles which made for dark moths would have spread rapidly in the population.

Using a little imagination we can think about two different parts of the world where this same event occurred independently - e.g. Glasgow and Plymouth in Britain which are quite far apart but both grew expansively during the industrial revolution. In both of these locations we would have seen a simultaneous rapid loss of lichens and increase in the dark moth ecomorph. This would have been convergent evolution because it is likely that they were independent of each other, i.e. the dark moth probably did not evolve in Glasgow and then fly itself down to Plymouth.


Techniques for detecting phosphorylation sites in proteins?

In principle X-ray crystallography or NMR could detect phosphorylation sites but they are much more complex and expensive techniques than mass spec. So for simply figuring out phosphorylation patterns in a protein is much easier using mass spec.

Detailed reasons:

For X-ray you need to crystallize the protein which is often very difficult/impossible and requires quite a lot of sample material. Afterwards you need a good X-ray source (ideally a synchrotron beamline) and record the scattering pattern over an extended range of angles (at least 180 degrees) before your crystal evaporates in the intense X-ray beam. Last but not least, you need additional chemical tricks, elaborate mathematical models and a large amount of computing power to compensate for the fact that in X-Ray crystallography you lose the phase information (because there are no suitable lenses for X-rays).

For NMR, you need large, very strong superconducting magnets, sophisticated radio transmitters and receivers, complicated math and computing power. However even if you have all that, you are still limited to very small proteins because otherwise the NMR spectrum is simply too complicated to be solved.

In contrast, for mass spec, you need a (highly sophisticated) spray gun, a moderate magnetic field and an electron multiplying detector. This is still a very sophisticated machine but much simpler compared to the above. In addition, data analysis is simpler than in the above cases.

Basically if you don't need to know the structural changes induced by phosphorylation (for which you would need to compare the structures of two crystals), you would stick to mass spec.


Are Bovine serum albumin, Avidin, Ficoll-70 and Dextran-70 positively charged or negatively charged?

For charge, you could check this one by sequence level, for example for Bovine Albumin (Uniprot: P02769) you can get the theoretical pI of 5.82, as the mean of pKa aminoacid values, to do this can use protparm, so when the pH > pI, the protein has a net negative charge and when the pH < pI, the protein has a net positive charge.

And there are only two organic polar solvents I known to work proteins, DMSO (pKa = 35) and
Dimethylformamide (DMF, pKa=-0.01 (20ºC))


What is the difference between these terms: clade, monophyletic group and taxon?

A taxon (Plur. taxa) is any (monophyletic or not) group of species. For example the group of yellow flowers is a taxon. The group of primates is a taxon. The taxon of aquatic animals is a taxon.

A clade is a monophyletic taxon or monophyletic group if you prefer. A monophyletic taxon (or a clade) is defined as a taxon that contains only all descendants of a common ancestor and the common ancestor. On the following picture, only the Taxon 1 is a clade.

To cite few examples of clades: Primates, Eukaryotes, Rosacea, Reptilomorpha, Rodentia. (The links yield to tolweb.org. See below for more info about this site)

A cladogram is some kind of reduced evolutionary tree that only shows the branching pattern but the length of the branches does not carry any information. At the opposite on a evolutionary tree the lengths of branches usually indicate the inferred time from the divergence.

I think the best tree you can find online is tolweb.org. You can find here the clade of Reptilomorpha and here the clade of Eupelycosaur. As you can see from these links, the mammals form a clade within the Eupelycosaur which itself is a clade within the Reptilomorpha. So yes, every human being is a Reptiliomorpha/Eupelycosaur/Mammalia. You can have fun going through this evolutionary tree and see what are the common ancestors between human and other mammals, human and turtles, human and jellyfish, human and plants, etc… to cite just a few relationships you might be interested to look at.


Why is dimethyltryptamine (DMT) being released during death?

The issue I suspect you are struggling with is the anthropomorphization of the evolutionary process.  Evolution is an optimization process driven by random mechanisms...i.e. there is often not a "reason" for why certain things are the way they are.  Evolution is not a conscious "designer" that produces things with a specific goal in mind...it simply "picks" the best random alteration and enhances it.  If there is no "best mutation", then there is no selection pressure to drive change overtime.

For example, one can ask, "Why do humans have 5 fingers on each hand, instead of 6 or 4?"  There is no answer, because the question itself is nonsensical.  Humans have 5 fingers simply because there is no pressure to drive a change to 6 or fingers, and so it boils down to randomness.  There is no "reason" humans have 2 arms, as opposed to 4.  That particular trait just randomly happened to be the one which became dominant.

So, to return to your question of "Why does the brain release DMT when dying?", the answer is that there IS no answer.  There is no selection pressure for or against that trait, it just happens.  As to the mechanism itself, I suspect that there is just a global breakdown of function in the brain, leading to a dump of ALL neurotransmitters.  When the reuptake pumps fail, the neurons just dump their contents into the extracellular space.  The result is pleasant hallucinations, giving the impression that humans are not "meant" to feel pain when dying.  Imposing that kind of rationale, however, is simply creating meaning out of chaos.  If you watch TV static long enough, your mind will start to see patterns which aren't there, simply because the human mind is "wired" to find patterns in chaos in order to better understand the environment.

To wrap this up, I suppose the answer to your question is that the brain is finding meaning in meaninglessness, simply because that is what the brain does.  We look for patterns to make sense out of our environment, which sometimes leads to spurious conclusions.  There is no reason that the brain hallucinates when dying, but there IS a reason that this trait appears to be a built-in mechanism.

I hope I was able to shed some light on the issue.  Or at the very least, not confuse you further :D


Is it theoretically possible to restore the Tiger population to 100,000?

I don't think your core question can be answered exactly, namely "...the theoretical maximum population to which the Tiger species could be restored", since there are too many variables to consider. However, the comment from @Remi.b is apt, in the sense that it shows that population growth rate per se (or reproductive rate) should not be the limiting factor. The bottleneck will probably be some concept of carrying capacity (the number of tigers that the current tiger habitats can sustain). This number will naturally depend on many factors, for instance whether all hunting of tigers and their prey is removed from the remaining habitats.

You could arrive at a ballpark estimate of the current "theoretical" maximum population size by finding the area of suitable tiger habitat and dividing this by the average size of tiger territories. However, the size of tiger territories differ quite a bit between males and females and between areas with different prey densities, and probably also between different tiger subspecies (which will covary with average prey density to some extent - Siberian tigers generally live in habitats with lower prey densities). Looking at estimates from the Smithsonian and wikipedia, territory sizes seems to range between 20 to 510 km2, with maybe even larger male territories in Siberia (so quite a big range). The IUCN Red list assessment of tigers state that the current tiger range is to 1.185 million km2 (from Sanderson et al. 2006 as "Tiger Conservation Landscapes"). It is however unclear whether this number corresponds to the total range extent or to the actual amount of suitable habitat (probably the former though). Nevertheless, lets say that the average territory size is 265km2 (probably way to high on average), that the estimated area from IUCN is correct, and lets assume that territories never overlap (which they do; male territories overlap with several female territories and female territories can also overlap to some extent). In that case, we will arrive at an estimated theoretical popultion size of ~4500 tigers. If we instead use a more modest territory size of 40km2 we will arrive at a population size of ~30000 tigers. Since territories can overlap, these estimates should be biased low, given their other assumptions.

Sanderson et al. (2006) however also includes a summary of "Effective Potential Habitat" of tigers, which sum to 5.65 million km2. If this number is used to calculate the estimated theoretical popultion size you will arrive at ~21300 or 141000 tigers, using the same territory sizes as above. However, this completely ignores issues such as landscape connectivity, and that tigers are completely missing from large parts of their former distribution (these factors, and others, were used to define the "Tiger Conservation Landscapes"). Also note that much of the potential habitat lies in low-productivity areas (Russia and parts of China), where territory sizes are relatively large.

Another perspective would be to use the historical population size pre-20th century and the amount of decrease in tiger habitat to estimate a theoretical population size. I don't know anything about the historical population size, but let's say that your 100000 is accurate (source?). Dinerstein et al (2007) state that current tiger ranges correspond to 7% of historical ranges. Using only these numbers, you could arrive at a current theoretical population size of 7000 tigers (100000*0.07), assuming that the tiger population should directly mirror the amount of available habitat. However, the current 7% of historical ranges include range contractions due to hunting, so this estimate should be biased low (maybe strongly so) with respect to the possible population size that could be obtained if all hunting stopped.

These calculations should show that the current Tiger populations could probably be increased quite a bit with strong and effective conservation efforts (in your words: if "poaching and habitat destruction stopped today and conservation efforts were increased drastically"), but that 100000 will probably be extremely hard to obtain, given that so much of the historical range has been lost. With reintroduction programmes and a long timeframe it doesn't appear to be impossible though, but this is ignoring potential future problems such as increased tiger-human conflicts. Also note that I don't know much about Tiger biology, that these are merely rough back-of-an-envelope calculations, and an expert could certainly give you a more detailed and accurate answer.

References:

Dinerstein et al. 2007. The Fate of Wild Tigers. Bioscience 57 (6): 508-514. doi: 10.1641/B570608
Sanderson et al. 2006. Setting Priorities for the Conservation and Recovery of Wild Tigers: 2005-2015. The Technical Assessment. WCS, WWF, Smithsonian, and NFWF-STF, New York – Washington, D.C.
The Smithsonian: Tigers
Wikipedia: Tiger
IUCN Red List: Panthera tigris


Why can't Turner Syndrome occur in males?

Because it is not viable to not have any X chromosome (non-peer reviewed reference).

The X chromosome is much bigger than the Y chromosome and carry a lot of essential genes (see here). A zygote just does not appear to be viable without X chromosome.


I'd say renewing refers to a constant process wheras regeneration applies to wholesale rebuilding due to trauma.

For example, your skin is constantly "renewed" by the undermost cells, adjacent to the basement membrane, dividing to produce new cells that migrate outward. These cells are modified to protect and eventually slough off to feed the mites in your bed. Ditto to cells lining the stomach which are replaced/renewed about ever three days due to abuse of stomach acid and salsa.

Humans can regenerate much of the last joint of a finger, bone and all. I'm not sure if this is age dependent nor how much of the knuckle needs to remain. Search "regeneration of fingers in humans" to find many references to this.


Where can I find the common names for the zoology taxonomy?

The Tree of Life project has a browse-able tree of all major taxa, but not necessarily all species. You can start at the root of the tree here. Tree of life uses modern phylogenetic nomenclature rather than more traditional Kingdom-Phylum-Class-etc.

Part of the problem that you will run into is that common names differ across regions/countries/languages. This is the point of species binomials. They are language-invariant.


Your gel looks just fine to me. It simply indicates that your ammonium sulfate precipitate contains massive amounts of this small protein at the bottom (whatever this is). The upper bands look fine, the amount loaded is appropriate: they are not overloaded like the bottom one, but not too faint either. The fact that your first and last lanes look a bit smeary is because of the massive amount of the small protein (lanes do look smeary when overloaded this much). The bottom band is definitely really some protein, and not a staining artifact; I have seen this shape before with purified proteins overloaded on SDS-PAGE.

One thing you could do, assuming you still have enough of these samples, is to run a complementary gel with 100 times less material. Dilute by a factor of 1/100 in 1X Laemmli denaturation buffer, and load a new gel with the same volume as for this one. You won't see the upper bands anymore, but you will have a much cleaner bottom band that you will hopefully be able to assign an apparent molecular weight to (or even cut out for mass spec identification; wear gloves and use clean tools if you do that, otherwise they will mostly detect keratin from your skin).

Assuming the point of this gel was to check the outcome of ammonium sulfate precipitation used as a purification step, well obviously it didn't work well to separate all these bands, and you might need to repeat and try different concentrations. But if the bottom band is the one you are trying to purify, then you were successful (the top bands represent less than 10% contamination, I would say by eyeball estimation). If you're interested in one of the top bands, then it clearly didn't work.

Is one of these lanes the supernatant? If so, you also have massive amounts of the small protein there (it's in every lane). Such a high enrichment looks suspicious: could that be purified lysozyme that you added during the purification procedure to help break down bacterial cell wall? (assuming you're trying to purify a protein over-expressed in E. coli).


Is there a correlation between B12 deficiency and cardiovascular disease?

Is it known whether low B12 causes cardiovascular diseases?

Yes, it is known. B12 deficiency does not directly cause cardiovascular disease, and I would be suspicious of any health site that says it does. B12 deficiency causes hematologic and neurologic problems.

  Why is low B12 correlated with high homocysteine:

Low B12 is correlated with high homocysteine because it is a cofactor for the conversion of homocysteine to methionine by homocysteine methyl transferase. Low folate will do the same thing (cause an elevation in homocysteine).

These cofactors and metabolites are involved in methyl donor reactions that are particularly important in the production of blood cells and myelin. Strict nutritional B12 deficiency (reduced intake) often occurs along with other nutritional deficiencies.

The primary hematologic problem is anemia, with associated changes in the morphology of certain white blood cells. The anemia, if severe and prolonged can contribute to cardiac problems of other causes. You also see paresthesias (often symmetric), a shuffling gait, and other odd neurological problems including depression and psychosis.  B12 supplementation does not always reverse the neurological problems.

You can read about B12 deficiencies in Cecil medicine Chapter 225 and 167, Harrison's Chapter 74, and in this review.


Why does anxiety cause diarrhea or constipation?

Hraish is right about the relationship between emotions and gut-brain axis. Stress hormones released by the brain are responsible for the gut-brain reflexes. Anxiety is related to stress and stress hormones are released when anxiety is expressed by the individual.

Irritable bowel syndrome(IBS)  symptom-based diagnosis, which is having symptoms such as chronic abdominal pain, discomfort, bloating, alteration of bowel habits, diarrhea, constipation etc.

  Irritable bowel syndrome (IBS) is a functional digestive disorder characterized by abdominal pain, bloating and altered bowel habits without any organic cause.

  (Drossman 1999b; Mulak and Bonaz 2004).

  In addition, stress is able to increase visceral sensitivity either at the central and/or peripheral level. (Mulak and Bonaz 2004; Larauche, et al. 2011).

Stress is enabled through the  corticotrophin-releasing factor (CRF) system (CRF, urocortins and their receptors CRF1,2), is a key factor involved in the pathophysiology of IBS.

  Stress is able to modify visceral sensitivity as well as GI motility, permeability, intestinal microbiota, and immunity of the GI tract, all mechanisms that are involved in the pathophysiology of IBS. In addition, stress is able to modulate the hypothalamic pituitary adrenal (HPA) axis and the autonomic nervous system (ANS) which is the link between the gut and the CNS and an imbalance of the ANS is observed in IBS patients. The main brain areas involved in stress are the prefrontal cortex, the limbic system (e.g. the hippocampus and the amygdala) and the hypothalamus. Relations between the prefrontal cortex and the limbic system are important in the management of stress response.
  (Pellissier, et al. 2010a; Mazurak, et al. 2012)

  One of the most common gut related conditions seen
  by GPs and Gastroenterologists is Irritable Bowel Syndrome (IBS), previously known as
  colitis,mucous colitis, spastic colon, and spastic bowel disease.Around 10-20% of adolescents and adults have symptoms consistent with IBS (with females twice as likely as males to report IBS symptoms).
  IBS is associated with 12 months of abdominal pain or discomfort which is (1) relieved with
  defecation; and/or (2) associated with change in stool frequency and/
  or form (i.e., constipation and/or diarrhoea). IBS is also associated with other gut-related symptoms including: bloating,nausea,and excessive gas. Non-gut related symptoms include fatigue, headaches, sleep problems,and pain conditions, such as fibromyalgia.

  Individuals who experience IBS also identify that their gut problems increase doing times
  of stress.Itcan become a vicious cycle-IBS is exacerbated by stress and stress is inturn increased by symptoms of IBS.With anxiety comes increased muscle tension around the gut
  (affecting gutmotility) and activation of the flight fight response, reducing blood in the gut (this is what causes butterflies in the tummy!). These physical changes cause the
  gut-brain to send signals to the brain which in turn promote further stress and distress, most commonly in the form of anxiety.For individuals with IBS (or actually most gut conditions), the ongoing worry about their gut and unproductive patterns can be very
  debilitating. It can also be the starting point for their anxiety
  and/or depression.
  Reference

From the above definitions it is clear that anxiety and brain-gut relationships are valid and IBS is an important reason for gut related disorders when stress is been experienced by the person. Over 10-20 % of adults have symptoms related to IBS, which means a common type of disorder in the general public.

  References

  Stress Affects the Amygdala Activity

  Anxiety and the Brain-Gut-Axis


How do Neurotransmitters get into the neurons?

The general rule (though like much of biology there are exceptions) is that each neuron releases a specific neurotransmitter: neuron types are often named by this principal neurotransmitter plus the suffix -ergic: a cholinergic neuron releases acetylcholine.

There are also similar molecules that do in fact act throughout the body, but we don't call these neurotransmitters, we call them hormones. Sometimes they are exactly the same molecule: epinephrine, also known as adrenaline, is both a neurotransmitter and a hormone; it can act as both because different receptors have different affinities, and the circulating hormone levels are typically much lower concentration than the amount that can be released in a more confined space.

Additionally, neurons have receptors for different neurotransmitters, so for example dopamine does not affect all neurons, only neurons that have dopamine receptors. Different cell types can also have different types of dopamine receptors, and those receptors can do different things to the cell. The same neurotransmitter could be excitatory to one cell and inhibitory to another.

Broad simplifications of nervous function such as:

  Dopamine is also known to increase our feelings of lust

really don't say anything broadly about the function of dopamine. I could similarly say that computers control airplanes: that statement is true even though you will fine airplanes not controlled by computers and because you will find the vast majority of computers don't control airplanes. However, if I turned off all the computers in the world, a lot of airplanes would have their function impacted.

How do neurotransmitters get into neurons?

Most neurotransmitters are synthesized within neurons from other ingredients. GABA, for example, is derived from an amino acid glutamate. Glutamate itself is also a neurotransmitter. All neurons that release neurotransmitters have pumps that concentrate these neurotransmitters into vesicles. Neurons often also have transporters to pull released neurotransmitter back into the cell so it can be reused, for example a common class of psychoactive drugs are the serotonin reuptake inhibitors: these drugs inhibit the protein that pumps serotonin back into serotonin-releasing cells.

General statement

Use of knowledge from neuroscience to improve AI algorithms has moved far beyond what a novice can contribute to. If you want to utilize biology in AI algorithms, you have to be prepared to become an expert in both. I'd suggest starting with a basic neuroscience textbook if you want to learn about neuroscience, for example books by Purves' Neuroscience or Kandell's Principles of Neural Science.


Why is black and yellow such a nice camouflage?

What makes a camouflage effective? It has to match the colors and color patterns of the habitat.

Here are two cheetahs

Here is another cheetah

Here is a leopard

Here is a jaguar

Overall, it looks like their yellow and black pattern is a pretty good camouflage.

The jaguar habitat is a mixture of open and forested habitats. One would think, the jaguar would gain by being a little greener but there is a good reason for the jaguar not being green (see Why is green fur not a thing?).

Note also that it would be a mistake to think that any species should be perfectly adapted to its environment. You might want to have a look at the paragraph Did you say Natural Selection? in this answer for a very short intro to why populations might sometimes be less adapted than a naive observer may expect. There might have an important phylogenetic signal among these felidae (you might to have a look at the paragraph Why 4 legs? in the same answer as indicated above).


Misunderstanding about nucleotide biosynthesis

A condensation reaction is defined on Wikipedia as

  a reaction in which two molecules or moieties, often functional
  groups, combine to form a larger molecule, together with the loss of a
  small molecule. Possible small molecules that are lost include water,
  acetic acid, hydrogen chloride, or methanol, but most commonly in
  biological reactions it is water.

It doesn't say anything about the number of steps required to reach the final compound, nor about the type of bonds formed. Following this definition, the nucleotide synthesis occurs via condensation reactions.


Why are beta-galactosidase proteins overexpressed in senescent cells?

Looking at the articles referenced in the Wikipedia article, there's probably no direct physiological link between senescence and beta-galactosides. Lee et al (2006) and others before them have shown that the "hypothetical" protein is just regular lysosomal beta-galactosidase, which is present in higher concentrations in aging and stressed cells because the number of lysosomes increase under those conditions. There's a collection of references in the Discussion section of the Lee paper that delves deeper into the aging-lysosome connection.

I'm well out of my depth by this point, but if I were going to take a wild guess I'd suggest that lysosomal upregulation could be part of a stress response involving autophagy (i.e. the cell breaking down and recycling intracellular materials to meet critical demands), though I don't know the specific connection to aging. As far as beta-galactosides go: if you have any hanging around, you get to eat them, is all, I bet. I bet the references in Lee would tell you if I'm on track or not.


Simple diffusion of lipid-soluble molecules through phospholipid bilayer -- does anything get "stuck" in transit?

I interpret your question to refer to the movement of a lipid-soluble molecule that is therefore able to diffuse into cells down a concentration gradient. I think that you are asking whether as the gradient collapses, some of these molecules would "stay in the bilayer".

You are thinking about the diffusion process in the wrong way. There will always be a pool of these molecules in the bilayer, and these will be continually exchanging with molecules in the two aqueous phases on either side of the membrane. The net flux which results in diffusion in any particular direction will be the  movement that results from these equilibria. Diffusion isn't a directed process in the way you define your question.

My diagram shows on the left the progress towards equilibrium and on the right the situation where it has been reached. Note that at equilibrium, because it is lipid soluble, the molecule is at a higher concentration (larger typeface) than it is in either aqueous phase. And - importantly, molecules will still be moving into and out of the bilayer at both faces.

Added later:
A classic example of a lipid soluble molecule able to diffuse in this way is oxygen. According to this paper, at physiological temperatures, and at equilibrium, the concentration of oxygen in a bilayer will be approximately 3x that in the surrounding fluids.