What is so difficult about mushroom cultivation?

What makes some mushrooms easy to cultivate is that they grow profusely, they aren't tree symbionts, where as sponge gilled culinary musrhooms are symbionts. Cheap mushrooms can easily be controlled with temperature and or light to fruit year round with minimal labour, they have cheap and easily obtainable substrate, and that are very appreciated for cooking and transportable. Also Argaricus doesn't even need light as a signal to trigger fruiting bodies and can be grown in complete darkness, and the harvest can be with robots not even manual, https://youtu.be/iBENPHl4mBA?list=PLw1YvKXHZymsoJbFGRI_OFSWZ5Wwg_fVD, which makes them particularly cheap.

Mycorrhizal mushrooms like boletes and many forest associated mushrooms differ from Argaricus and
commonly commercially produced saprotrophic
types (such as shiitake and button mushrooms).
Saprotrophic mushrooms live and feed on dead
organic matter, whereas mycorrhizal mushrooms
grow in a close, symbiotic (mutually beneficial)
relationship with the living roots of a tree.

Field and dead wood mushrooms generally have simpler substrate that can be transported in boxes in the dark, and almost all cultivated mushrooms are of saprotrophic.

Saprotrophic nutrition /sæprəˈtrɒfɪk, -proʊ-/ or lysotrophic nutrition is a process of chemoheterotrophic extracellular digestion involved in the processing of dead or decayed organic matter. It occurs in saprotrophs or heterotrophs, and is most often associated with fungi (for example Mucor) and soil bacteria.

That's slightly different to Saprophytes are more generally plants which live on dead or decomposing matter and which can also be more accurately be called myco-heterotrophs because they actually parasitize fungi, rather than dead organic matter directly.

They say that Argaricus was first discovered in 1650 on melons! but as any theory, there were probably precedents. Any farmer that discovered sizeable populatons of fungi near horse and cow middens could have easily have experimented with placing some compost in a basement.

Morelles and truffles are such expensive mushrooms that the man who learns how to grow big truffles will be payign himself up to a 1000 dollars a kilo for his efforts, it illustrates the difficulty of micorrhizal cultivation.

If you are interested in fungi there is a fascinating ted talk about them from Paul Stamets.

and
https://en.wikipedia.org/wiki/Mycorrhiza


How does Acetaldehyde accelerate mitosis?

First of all Alcohol and Acetaldehyde are both cytotoxic. Along in our development we learned to deal with both substances, which is shown by specific metabolism pathways to break them down (for example alcohol dehydrogenase, acetaldehyde dehydrogenase, Cytochrom P450 and so on).

Alcohol and Acetaldehyde both have a negative effect on mitosis (which explains a good part of the negative effect which alcohol has on developing embryos).
Examples can be the following articles:

Acetaldehyde causes a prolongation of the doubling time and an
increase in the modal volume of cells in culture.
Alcohol inhibits cell mitosis in G2-M phase in cell cycle in a human
lymphocytes in vitro study.
Ethanol induces transient arrest of cell division (G2 + M block)
followed by G0/G1 block: dose effects of short- and longer-term
ethanol exposure on cell cycle and cell functions.
Ethanol induction of sister chromatid exchanges in human cells in
vitro.

Alcohol also has some effect on cancer - probably not by directly causing it, but at least as an additional risk factor. One article I found ("Alcohol and Cancer") mentions the following possibilities:

  The mechanisms by which alcohol consumption exerts its carcinogenic
  effect have not been defined fully, although plausible events include:
  a genotoxic effect of acetaldehyde, the main metabolite of ethanol;
  increased oestrogen concentration, which is important for breast
  carcinogenesis; a role as solvent for tobacco carcinogens; production
  of reactive oxygen species and nitrogen species; and changes in folate
  metabolism.

Using Pubmed you can find more articles on that topic.


There are a number of different wiring scenarios that could lead to this type of behavior, even in a dissociated neuronal cell culture.  The two major cases are neurons that are truly isolated from each other, and collections of neurons that connect together.  Since your question refers to firing and synchronized bursts, I'll restrict my discussion to the generation of spontaneous action potentials - but keep in mind that not all synaptic communication requires an action potential (the vast majority of internal connections within the retina, for example)

In the case of ensembles neurons in vitro, spontaneous activity is fairly typical.  One simple way to get this activity is for a subset of cells in the network to be inherently spontaneously active.  In the case of single, isolated neurons, this kind of individual cell spontaneous activity could also result in a single neuron firing spikes in a periodic fashion.  So for example purposes, let's explore how a single cell could produce this kind of activity.

Since action potentials are triggered by a sufficiently strong depolarization, we need to identify potential membrane polarizing sources.  When dealing with single cells, the major controllers of cell membrane voltage potential are the voltage gated ion channels.  When open these channels can cause, depending on their type and cellular/extracellular conditions, either a depolarization or hyperpolarization in the cell.  And, most interestingly, whether they are open or not depends on the cell membrane's polarization state.

That makes voltage gated channels excellent at feedback:

a depolarizing channel that is depolarization gated will further activate itself once activated, leading to yet more activation.  This is a positive feedback cycle.
a hyperpolarizing channel that is depolarization gated will, upon depolarization of the cell open and serve to hyperpolarize the cell until the initial depolarization has been removed.  In this way it would serve as a negative feedback source.

Physiologists have thoroughly characterized many of these cells, and they have many more states beyond an "open" and "closed", such as different levels of "inactivated".  But we don't need to know about those to answer your question.

The last piece we do need is brownian motion which is the movement of particles due to their bombardment by other particles.  This motion can with some frequency cause voltage gated channels to spontaneously open or close, which introduces noise into the system.

As you can imagine, if you have a positive feedback channel that is gated spontaneously, it will make it briefly more likely for other depolarization gated channels to be activated.  Positive feedback can quickly lead to a rapid depolarization of the cell, which could be observed as a burst of spikes.  If you include a set of slower reacting depolarization gated hyperpolarizing channels, then it's easy to construct a scenario where the cell would depolarize spontaneously with no apparent input, then have a quiescent period where a prolonged hyperpolarization makes it less likely to fire spontaneously.

Voila, bursting in an isolated neuron.  Place a set of those neurons in a network and you can get generate a lot of spontaneous activity.


Difference between pulse and blood pressure

The blood pressure is the fluid's movement "strength" in the
  arteries (or "artères", please edit my post with the correct english word)

Blood pressure is a measurement of the strength of flow through the arteries. (I.e., the force per unit area exerted by the blood on arterial walls.) So replace vein with artery and your definition is correct.

  The "tension" is the force applied on the veins itself, kind of like
  when you're pulling a rubber band

In cardiovascular terminology, hypertension and hypotension are used interchangeably with high and low blood pressure (even though technically tension uses force units and pressure uses force/unit area units). Your definition sounds more like arterial tensile strength, which is the ability of the artery to withstand pulling forces without breaking (which decreases with age).

  The pulse is just the wave of blood moving, which creates different
  tensions over the vein and whose movement is created by the pressure.

Pulse is an indirect measurement of heart rate. So, yes, it's the rate of the "wave of blood moving." It creates different "pressures" measured by systolic (the "wave" in your terms) and diastolic (the "trough") whose movement is created by the force (of the heart walls contracting).


How many consecutive cell divisions are required to form the adult human body from the single cell zygote?

Sounds like just a math problem if you allow that cells dying and different rates of division are not to be accounted for:

$2^N = 40 \times 10^{12}$

$log_2(40 \times 10^{12}) = N$

$N = 45.185$

so 45 or so divisions.

is that what you are looking for?


Why do we suddenly forget things, like PIN or phone numbers, that we've known for years?

Forgetfulness is a common phenomenon that tends to increase with age. It usually affects short term memories but it can affect long term ones too. Here are some possible causes which I quote from Healthline (the full list available at that link):

  sleep deprivation
  use of alcohol or drugs and some prescription medications
  lack of oxygen to the brain
  migraine

It can happen at any age and it is normal if (quoting Deane Alban, Memory Loss: When It’s Normal and When It’s Serious):

  Are you overworked and stressed out? Are you eating poorly? Are you on a low-fat diet or skipping meals to lose weight?  Do you struggle with insomnia? Do you drink too much?

  If you answer “yes” to any of these questions, it’s likely you are losing your memory because your lifestyle is catching up with you.

You mention loss during sleep in your question. Sleep affects memories (see WebMD and Wikipedia):

deprivation of sleep leads to memory loss
during sleep brain selects relevant information gathered during the day and turns it into memories
certain stages of sleep improve memories


What species is this yellow flower of angiosperm from Morocco?

It's undoubtedly in the genus Oxalis but there are hundreds of species in this genus.  The genus name refers to the high content of oxalic acid found in this genus.


What is the meaning of "The Molecular Basis of Disease"

There is an ELSEVIER research journal by the name of BBA Molecular Basis of Disease (link to journal). I think their synopsis of what the journal is about will illuminate what is meant by The Molecular Basis of Disease.

  BBA Molecular Basis of Disease addresses the biochemistry and
  molecular genetics of disease processes and models of human disease.
  This journal covers aspects of aging, cancer, metabolic-,
  neurological-, and immunological-based disease. Manuscripts focused on
  using animal models to elucidate biochemical and mechanistic insight
  in each of these conditions, are particularly encouraged.

The keywords here are biochemistry and molecular genetics, so I would think of what kind of mutations, at what chromosomal locations can cause genetic disorders for example. Or in terms of biochemistry, what kind of biochemical environment can lead to alcoholic liver disease etc.


Should be a Papaya, thus a fruit, an outline of your geographical location would be helpful to determine it.


Dimethyltryptamine and Sigma 1-type opioid receptor interaction

From your article:

  Sig-1Rs localize at the interface between the endoplasmic reticulum (ER) and mitochondrion, which is known as the mitochondria-associated ER membrane (MAM).

Consequently, they are found in a variety of areas within the central nervous system as well as in other types of cells throughout the body (notably cardiac cells).

  An important biological activity of sigma receptor activation is the inhibition of ion channels, which operates through protein-protein interactions without mediation by G proteins and protein kinases. In addition to modulating various types of voltage-activated K+ channels, the sigma-1 receptor associates with the Kv1.4 K+ channel in posterior pituitary nerve terminals, as well as in Xenopus oocytes. Sigma receptor ligands also modulate N-, L-, P/Q-, and R-type Ca2+ channels in rat sympathetic and parasympathetic neurons. Sigmareceptor ligands modulate cardiac voltage-gated Na+ channels (hNav1.5) in human embryonic kidney 293 (HEK293) cells, COS-7 cells, and neonatal mouse cardiac myocytes. To evaluate the capacity of DMT to induce physiological responses by binding to sigma receptors, we examined the action of DMT on voltage-activated Na+ current.

From:

  Fontanilla D, Johannessen M, Hajipour AR, Cozzi NV, Jackson MB, Ruoho AE. The hallucinogen N,N-dimethyltryptamine (DMT) is an endogenous sigma-1 receptor regulator. Science. 2009;323:934–937.  [DOI]
  (reference 24 in the article that you cite)


Constantly wiggling moth pupa - will it emerge soon?

I posted the same question on tumblr and got an answer:

  It depends on the species. This one looks like a Noctuid. I’d give it
  two weeks to a month or so. You may be able to see its wings showing
  through the darkening pupal case when the time draws near! Just make
  sure you give it somewhere to climb up and expand its wings when it
  ecloses.

After keeping it until the moth emerged, I now know that wiggliness is not an indication of maturity, but turning dark is.


I personally like to talk in Morgan (M), instead of centiMorgan (cM), because the Morgan has a more intuitive meaning than one-hundredth of its value.

Morgan

If two loci are at distance 1M, it means the expected number of cross-over happening between these two loci is 1. If they are at 0.1M, then the expected number of crossover is 0.1. If they are at 1.4M, then the expected number of crossover is 1.4.

centiMorgan

As the typical distance of interest is much lower than the Morgan, we typically talk in centiMorgan.

Rate of recombination

If in a given meiosis, there is 0 crossover between two loci, then the two alleles from the same haplotype will end up in the same gamete. If there is 1 crossover, then the two alleles from the same haplotype end up in different gametes. If there are 2 crossovers between two loci, then the two alleles from the same haplotype will end up in the same gamete.

In short, if the number of crossovers between two loci (which expected value is the number of Morgans) is even, then the two alleles from the same haplotype will end up in the same gamete.

At very low Morgan (say 0.000001M), the probability of having an odd number of crossovers is low and the recombination rate is therefore low. As the number of Morgans increases, this probability of having an even number of crossover approaches 0.5. The recombination rate can therefore never be greater than 0.5.

Physical distance

Note that as the recombination rate per nucleotide varies throughout the genome (and among genders and among lineages), the distance in Morgan between two loci is not a simple function of their physical distance in number of nucleotides. The two are obviously correlated though.

Human genome

In the human genome, the average per nucleotide recombination rate is of the order $5\cdot 10^{-8}$ (Wang et al. 2012). This means that 1 cM is about 1.5 millions of nucleotides.

Highly Related posts

This question has actually been answered several times already. You'll find more information, some drawings and some math at the posts

Recombination frequencies
Genetic linkage greater than 50 centimorgans

For a more introductory post, have a look at

Why do we need two markers to measure a recombination rate?


Why do sloths come down from the trees to defecate?

From Wikipedia:

  Sloths go to the ground to urinate and defecate about once a week, digging a hole and covering it afterwards. They go to the same spot each time and are vulnerable to predation while doing so. The reason for this risky behaviour is unknown, although some believe that it is to avoid making noise while defecating from up high that would attract predators. Consistent with this, they reportedly relieve themselves from their branches during storms in the rainy season. Another possible explanation is that the middens provide the sloths with one of their few methods of finding one another for breeding purposes, since their sense of smell is far more acute than their eyesight or hearing. It has also been pointed out that individual sloths tend to spend the bulk of their time feeding on a single "modal" tree; by burying their excreta near the trunk of that tree, they may help nourish it. [Source]


What are the "stars" we see after a bump on the head?

"Seeing stars", or as it formally is called, "phosphene", is caused by stimulation of the visual cortex or retina by causes other than light hitting the retina.
http://www.oubliette.org.uk/Three.html


Basic Amino Acid Residue Binding Mechanism to DNA

This question has no particular answer.  There are several families of DNA binding proteins, some of them bind specifically (e.g. restriction enzymes like EcoRI which binds to and cuts GAATTC or transcription factors like lac repressor which binds a particular point of the e coli genome about 25 base pairs long) and some of them bind semi-specifically (e.g. zinc fingers which bind GC rich regions), others non specifically (e.g. the sliding DNA clamp).

For all of these proteins, they will have a tendency to have positively charged amino acids facing the DNA because the DNA's phosphate backbone is negatively charged.  There are lots of protein motifs (like the helix turn helix motif) that fits into the major or minor groove of the DNA.  The lysine and argenine are important because they are the positively charged amino acids.  Histidine is also positively charged, but it is not as long and flexible, and doesn't seem to fit as often or as well.

http://en.wikipedia.org/wiki/DNA-binding_protein


Do butterflies pass over migration patterns to their offspring?

If you think about it, monarchs must have a pretty strong genetic component to migration since often they only make one round trip at most in a lifetime. But its not as simple as passing a map in the DNA.

If a mountain springs up on the route, the 'common sense' of the butterflies are still operational and they will tend to find their way around it.

The paper discussed here is older.  More recent Monarch butterfly migration  of some genetics that have been done shows some traits that are related to migration patterns by sampling over many butterflies whose patterns vary tremendously.

Glancing over the paper, I'd say that there may be some 'muscle' memory in migration, but probably the mechanisms encoding the route of migration are not yet discernable.  This is far from something we understand well.

The insect is following patterns of behavior but doesn't turn into a robot just because its migrating.  Migration patterns are probably linked to a series of environmental cues.

Changes in climate or shifts in magnetic fields can change migration patterns. Butterflies would be very different than say migratory birds in terms of the social and environmental markers for migration.


Meaning of "primers IL-2" in a scientific article

From the description, yes, those primers are supposed to be specific for the IL-2 gene. The way they would be used would be on mRNA, not DNA, so you could use them to quantify the level of IL-2 transcription. However, there seems to be some glitch in there, because while the first sequence (5′-CAGCTGTTGCT GGACTTACAGG-3′) matches rat IL-2 mRNA starting at 120 in the sequence,  the second one (CACAGTTGATGGCTCATCATCG) does not match any IL-2; a BLAST search only turns up random and irrelevant matches.

This may be an error in the paper (copying and pasting the wrong primer, which is extremely common, unfortunately); it may have been an error in design (someone used the wrong primer and got lucky results that seemed to match what they expect); or I may be doing something wrong, which I'm not going to try to troubleshoot any more than this.

(Edit, as @VonBeche points out in comments the reverse primer is almost a match at 398, with a one-nucleotide mismatch that screwed up my search -- possibly allelic variant, but equally possibly a mistake)


What is the film that covers the tongue?

It isn't really a film. The tiny bumps that cover your tongue are called papillae, and are normally pink in color. However, they can become inflamed and white when irritated. The appearance of the white "coating" is caused by debris, bacteria and dead cells getting lodged between the papillae.

You may be breathing through your mouth when you sleep, which is drying it out. Bacteria may also still be the cause; you may not be brushing well enough or your toothpaste may not be correctly doing its job.

The color variations may be due to different types or amounts of debris, or the color may vary with different conditions listed here. Tongue color changes also often occur with glossitis (inflammation of the tongue itself).


What is the scientific name of this plant?

The plant is of Lamiaceae family and its common name is Shell Flower or Bells of Ireland.

Its "scientific" aka latin name is Moluccella laevis.


What is the function of clot retraction?

The platelets in the clot contain contractile proteins. They bring the edges of the wound together, which also reduces the chance of further bleeding. The contraction process also supports the wound healing process as it brings the ends of the wound together.

For more information see this article: "Mechanics and contraction dynamics of single platelets and implications for clot stiffening"


What does "novel, predicted deleterious, within autozygome" mean in genetics?

For a genetic variant:

novel - Not previously reported in the scientific literature.
predicted deleterious - There are reasons to suspect the variant could cause abnormal effects in a person.  This may be in part from where the variant is located (e.g. what gene), what problems were observed in persons having the variant, and many other considerations.  See the "Variant interpretation" section of this paper for more detail.
in autozygome - "Autozygous" refers to parts of the genome which are identical on both maternal and paternal chromosomes because of common ancestry of the two parents.  The autozygome is the collection of all such segments for a person, and is larger in cases of inbreeding, as when the parents are first cousins.  Autozygous segments are (usually) entirely homozygous, that is, all alleles are the same since they come from the common ancestor. (In normal segments, there will be a mix of matching and mismatching alleles.) The importance of homozygous alleles, of course, is that a recessive allele will be expressed in the person when both alleles are the same.  (Related papers: "Autozygosity mapping with exome sequence data", "Autozygome-guided exome sequencing in retinal dystrophy patients reveals pathogenetic mutations and novel candidate disease genes".)


Why are victims of Covid19 being wrapped in plastic?

The WHO guidelines for VHF victims (Ebola etc.) do say that they should be buried in body bags, and if those are not available, in plastic sheeting.

  If body bags are not available, wrap the body in two
  thickness of cotton cloth and soak with 1:10 bleach
  solution. Then wrap the body in plastic sheeting. Seal the
  wrapping with plastic tape. Spray the body bag as in
  Step 3. Place the body in a coffin if one is available.

Obviously some are treating covid-19 victims with the same amount of caution. I can't tell you at the moment if this is justified or not.


Why is oxygen used up in eutrophication?

Algae produce O2 in the upper layer of water but when they die they stop producing O2. They sink to the seafloor and most get decomposed by bacteria on the seafloor. In this process, bacteria use O2 contained in the bottom layer of water which decreases the dissolved O2 concentration in the bottom water.

These concepts (and much more!) are well described in the excellent open-access paper by Rabalais et al. (2010) Dynamics and distribution of natural and human-caused hypoxia. It also includes case-studies of areas affected by hypoxia and eutrophication around the world. A must read if you're interested in this topic!


Why does non-continuous sleep makes you feel tired?

Sleep is not homogenous - there are different phases of sleep - REM, NREM-1 to NREM-4. And these different stages may play different roles in 'rejuvenating' the body (as you put it).

When you first fall asleep, you go into NREM-1 phase, which is the lightest sleep, and progresses into NREM-4, and for the first half of your sleep cycle, this cycles so you go from NREM-1 > NREM-2 > NREM-3 > NREM-4 > NREM-3 > NREM-2 > ....

On the first half of your sleep cycle, the NREM3 and NREM4 phases dominates, only on latter half of your sleep cycle are REM phase observed and progressively dominate.

Depending on how much you are waken up by, once you escape your sleep cycle, you may re-enter back at a different stage, which may mean you are no longer able to have much REM sleep. Subsequently, you will not have the rejuvenation that is associated with REM sleep and you feel tired.

Interesting note: There are people who have tried a method called polyphasic sleep, where they nap/sleep periodically and regularly, instead of sleeping once a day for 8 hours, say. People who promote this says that people do not feel tired because as soon as they nap, they go in REM sleep, and so the amount of REM sleep you get per day will still be the same. I'll let you make your own mind up about this one.


In ketogenesis, why is acetacetyl-CoA not directly hydrolized to acetoacetate in ketogenesis?

I believe it is related to the fact that the enzyme HMG-CoA lyase is regulated by glucagon (activates) and insulin (inactivates). It appears that this extra step was added so the pathway can be hormonally regulated.


Self-thinning: slope of log (biomass) vs log (density) is -1/2 whereas slope of log (weight) vs log (density) is -3/2, why?

Biomass here refers to the total mass of all the organisms in the population (in a unit of area), added together.

Weight here refers to the average weight or mass of an individual.

If biomass decreases, that could be because the individuals got lighter, or it could be because there are fewer of them, or both.

Added

I think I see what's happening.

Let $W$ be the average mass of an individual, $N$ be the number of individuals, and $B$ be their total biomass. Then of course,

$B=WN$

Let's start with:

$W$ is proportional to $N^{-\frac{3}{2}}$
$N$ is proportional to $N$ (duh). Let's rewrite that though, as:
$N$ is proportional to $N^1$

But that means:

$B=WN$ is proportional to $N^{-\frac{3}{2}} \cdot N^{1} =N^{-\frac{3}{2}+1} = N^{-\frac{1}{2}}$

Density increases with density (N). Weight per individual  decreases with the -3/2rd power (W). So their product, biomass decreases with the -3/2 + 1 = -1/2nd power  (B=WN).


What is the name of this yellow bumble bee that I photographed in New York City?

It's a Brown-belted Bumble Bee (Bombus griseocollis).

Details: http://bugguide.net/node/view/3538


Interesting hypothesis! - all of those animals you mentioned in fact do have ears, they just don't have external pinnae. You are probably thinking of these external structures when you are thinking of ears.

Importantly, pinnae are unique to the mammals, and not even all mammals have them. Since most mammals do not lay eggs, that is probably the joint relationship you are recognizing. Monotremes (egg laying mammals) also don't have external pinnae (for example see this book). So, the scientific reason is that both non-egg laying and external pinnae evolved in the mammalian lineage around the same time.

I don't know of any shared benefit for these traits to go hand-in-hand, but you could probably come up with more traits that also largely follow these ones, again because of shared lineage rather than a particular synergy.


1) Pareas iwasakii has asymmetric mandibles.  A few more examples of asymmetric snakes (reference)

Pareas iwasakii skull

2) Camels have an asymmetric penis (reference)

3) You could find quite a few in this article titled Animal asymmetry

Hope that helps. I am sure there are more but these are some I could find.


I think Feynman is referring to the second law of thermodynamics.

The entire statement is this:

  The most important feature of the cycle of Fig. 3–1 is the transformation from GDP to GTP (guanosine-di-phosphate to guanosine-tri-phosphate) because the one substance has much more energy in it than the other. Just as there is a “box” in certain enzymes for carrying hydrogen atoms around, there are special energy-carrying “boxes” which involve the triphosphate group. So, GTP has more energy than GDP and if the cycle is going one way, we are producing molecules which have extra energy and which can go drive some other cycle which requires energy, for example the contraction of muscle. The muscle will not contract unless there is GTP. We can take muscle fiber, put it in water, and add GTP, and the fibers contract, changing GTP to GDP if the right enzymes are present. So the real system is in the GDP-GTP transformation; in the dark the GTP which has been stored up during the day is used to run the whole cycle around the other way. An enzyme, you see, does not care in which direction the reaction goes, for if it did it would violate one of the laws of physics.

Now, there are some mistakes here. For instance, GTP is not used in the muscle contraction but ATP. Perhaps this was not quite known during Feynman's times. Coming to the point, I think what Feynman means is that external work has to be done by the enzyme (that catalyses the GTP-GTP exchange) if it is actually moving the chemical equilibrium towards one side (against what would happen in an uncatalyzed condition). Some enzymes can actually do that (shift equilibria and catalyse one sided reactions), by using energy from ATP hydrolysis or other energetic transformations but since they are performing work by using energy from an external source, they are also not violating the second law.

That's the essence of the second law of thermodynamics: you cannot move heat from a cold reservoir to a hot reservoir unless external work is done. We don't have "heat" here but there concept is the same for chemical energy and reaction rates.


Reptiles are a paraphyletic group because?

I think the question's phrasing is arguably a little wobbly, typically as to the nature of what someone would mean by the term "reptile". But I think you understood what your teacher was expecting. I agree with you, answer is B.

Reptilia is a clade (clade = monophyletic group) that encompasses all species that we traditionally classify as reptiles + all birds. Hence, our traditional definition of reptile makes up for a paraphyletic group as birds aren't included.

Related post: If dinosaurs could have feathers, would they still be reptiles?


Is there a resource that has quantitative data about cell proteins?

I'll list the papers that I obtained these parameters from. BioNumbers is a very useful resource and some of these papers that I cite have been obtained from the reference mentioned in BioNumbers. So BioNumbers should the first place to look for things like this. If you are not satisfied then start googling around :)

You should, however, keep in mind that simulation using exact parameters may not be very helpful. You can try varying the parameters in some given range and see the effects. Some parameters actually vary a lot.

Protein translation rate: 11 amino acids per second. Assume some steady state concentration of mRNA. This parameter is highly variable as there can be multiple ribosomes per mRNA [1]. Also see Schwanhäusser et al. (Supplementary excel sheet) [2]
Protein degradation rate: Take an average or one of the values reported by Schwanhäusser et al. (2011) [2]
Association/dissociation rates: See table shown by Zhou (2003). It lists different known interactions.[3]
Protein diffusivity: This differs for cytoplasm and water. You can assume diffusivity in ECF to be same as that in water. See Arrio-Dupont et al. (2000) [4]. They report it for specific proteins. You can extrapolate for other proteins using the Stoke-Einstein relation which says that diffusivity decreases inversely with the radius of the particle.

[1] Siwiak, Marlena, and Piotr Zielenkiewicz. "Transimulation-protein biosynthesis web service." PloS one 8.9 (2013): e73943.

[2] Schwanhäusser, Björn, et al. "Global quantification of mammalian gene expression control." Nature 473.7347 (2011): 337-342.

[3] Zhou, Huan‐Xiang. "Association and dissociation kinetics of colicin E3 and immunity protein 3: convergence of theory and experiment." Protein science 12.10 (2003): 2379-2382.

[4] Arrio-Dupont, Martine, et al. "Translational diffusion of globular proteins in the cytoplasm of cultured muscle cells." Biophysical journal 78.2 (2000): 901-907.


Does Cas9 require a nuclear localization signal (NLS) for it to work in a Eukaryote?

The transport from cytoplasm to nucleus is mediated by importin family. Importion family recognize NLS and transport proteins such as transcription factors into nucleus. So, NLS is necessary for cas9 to be transported into nucleus.


Can monoclonal antibodies be used to transport insulin

Technically you can link two proteins together, but why would you want to do this?
Antibody drug-conjugates are used to specifically target cells which can be differentiated from the healthy cells by their cancer neoantigens. This provides a high specificity of the drug delivery and also limits side effects on healthy cells.

For insulin on the other hand this is not necessary, since insulin receptors are ubiquitous thoughout cell surfaces in the body, hence supplementing insulin is enough.


Is the Amazon forest O2 and CO2 neutral?

tl;dr We don't really know. A reasonable guess is that it's a weak sink, gradually turning into a source via increased drought frequency, but it's extremely hard to measure; carbon flux is highly variable both spatially and temporally (so it matters both when and where you measure), and it's difficult to make sure that you're accurately measuring all the different components of carbon flux.

Dolman and Janssen 2018 say:

  Ground observations suggest that, through tree growth, the Amazon forest acts as a net carbon sink to the atmosphere (Brienen et al 2015), which is confirmed by atmospheric studies (Gatti et al 2015). However, the sink strength appears to have been declining since the 1990s and recent drought events in 2005, 2010 and 2015 might have temporarily reversed the Amazon carbon sink into a source (Feldpausch et al 2016, Gatti et al 2015)

They go on to discuss the great difficulties in constructing an accurate model of Amazonian carbon dynamics (for the purpose of predicting future source/sink relationships).

Rice et al. 2004

summary based on measuring living trees and coarse woody debris [CWD], it looks like a particular patch of forest was a small net source, but this may be a transient effect.

  Amazon forests could be globally significant sinks or sources for atmospheric carbon dioxide, but carbon balance of these forests remains poorly quantified.

In other words, "it's still unclear [as of 2004], so we did another study."

  We surveyed 19.75 ha along four 1‐km transects of well‐drained old‐growth upland forest in the Tapajós National Forest near Santarém, Pará, Brazil (2°51′ S, 54°58′ W) in order to assess carbon pool sizes, fluxes, and climatic controls on carbon balance.

So they took a very small sample of a particular forest type.

  The gain in live wood biomass was exceeded by respiration losses from CWD [coarse woody debris], resulting in an overall estimated net loss from total aboveground biomass ...

So this particular patch of forest was a carbon source at this particular time ...

  ... a period of high mortality [probably] preceded the initiation of this study ... transfer of carbon between live and dead biomass pools appears to have led to substantial increases in the pool of CWD, causing the observed net carbon release.

... but that may be due mostly to a recent die-off - maybe not true over a longer time scale ...

  ... the hypothesized sequestration flux from CO2 fertilization ... would be comparatively small and masked for considerable periods by climate‐driven shifts in forest structure and associated carbon balance in tropical forests.

... it will probably bounce around a lot (i.e., it's not wise to extrapolate this result either in space or time).

Miller et al. 2004

  We used two independent approaches, biometry and micrometeorology, to determine the net ecosystem production (NEP) of an old growth forest in Pará, Brazil. ... Biometric inventories indicated that the forest was either a source or, at most, a modest sink of carbon from 1984 to 2000 ... biometric and micrometeorological measurements in tandem provide strong evidence that the forest was not a strong, persistent carbon sink during the study interval.

and a more recent reference ...

Antonucci et al. 2018

  The objective this paper was to quantify the hourly variability of CO2 fluxes in the year of the El Niño, in 2015, in a tropical rain forest in the Western Amazon ... The average daily behavior of CO2 fluxes showed higher concentrations of absorption during the day than emissions overnight, behaving as a carbon sink, corroborating the importance of the forest in assimilation of the atmospheric carbon.

references

Miller et al, "Biometric and micrometeorological measurements of tropical forest carbon balance". Ecological Applications 2004, https://doi.org/10.1890/02-6005
Rice et al., "Carbon balance and vegetation dynamics in an old-growth Amazonian forest". Ecological Applications 2004, https://doi.org/10.1890/02-6006
Antonucci et al, "CO2 fluxes in a wet tropical forest area in Western Amazon in year of El Niño". Ciência e Natura, v. 40, 2018. https://periodicos.ufsm.br/cienciaenatura/article/view/30718
Dolman and Janssen, "The enigma of the Amazonian carbon balance", Environmental Research Letters 2018. https://iopscience.iop.org/article/10.1088/1748-9326/aac78e/meta


Meaning of "auto" in trans autophosphorylation?

Receptor tyrosine kinases are proteins which float around in the cellular membrane. Upon binding of their ligand, the dimerize (two units form a dimer). This releases the kinase domains and the proteins start phosphorylating themselves over cross (meaning part a phosphylates part b and vice versa). This looks like in this figure below (from here, it is an interesting article):

Besides ATP this process needs no further co-factors so the "auto" refers to the ability of the RTK to phosphorylate itself upon activation. See more about autophosphorylation here.


How does gene affect organs development in eukaryotic cells?

The question is very broad and I think can only be answered in very broad terms.

Proteins have metabolic functions. They do stuff! Their actions include catalyzing metabolic reactions, transporting molecules (incl. transport through the membrane), DNA replication, response to external stimuli and many other functions. Humans synthesize almost 30,000 different proteins Muller et al. (2002). The sum of their action put into a specific environment (such as a womb for mammals) end up building up and maintaining an individual.

Let's consider for example Hox genes. From wikipedia

  Hox genes, a subset of homeotic genes, are a group of related genes that control the body plan of an embryo along the head-tail axis. After the embryonic segments have formed, the Hox proteins determine the type of appendages (e.g. legs, antennae, and wings in fruit flies) or the different types of vertebrae (in humans) that will form on a segment. Hox proteins thus confer segmental identity, but do not form the actual segments themselves.

For more information, I would recommend you to have a look at an intro course to developmental biology. You might want to learn about HOX genes


Are there enzymes found in nature or the man made world that can help break down metals?

There are bacteria, which can assist the proces of rust.

"Some sulfate-reducing bacteria produce hydrogen sulfide, which can cause sulfide stress cracking. Acidithiobacillus bacteria produce sulfuric acid; Acidothiobacillus thiooxidans frequently damages sewer pipes. Ferrobacillus ferrooxidans directly oxidizes iron to iron oxides and iron hydroxides; the rusticles forming on RMS Titanic wreck are caused by bacterial activity. Other bacteria produce various acids, both organic and mineral, or ammonia." (http://en.wikipedia.org/wiki/Microbial_corrosion)

As you see, many of these active ingredients, like hydrogen sulfide, sulfuric acid, other acids or ammonia are not enzymes per se, although they are produced by enzymatic processes in bacteria.

Closer to your specification is Ferrobacillus ferrooxidans (synonyms: Acidithiobacillus ferrooxidans, Thiobacillus ferrooxidans, Ferrobacillus sulfooxidans), which directly acts on iron by enzymes associated with the cell membrane:

Valid XHTML http://c431376.r76.cf2.rackcdn.com/18185/fmicb-03-00096-HTML/image_m/fmicb-03-00096-g001.jpg.

Figure 1. Schematic representation of ferrous iron oxidation by the Gram-negative autotrophic acidophile, At. ferrooxidans. Controlled influx of protons is used to generate ATP via the membrane-bound ATP synthetase complex (ATPase). Iron oxidation is mediated by a cytochrome located on the outer membrane and electrons transferred via periplasmic cytochromes and rusticyanin either to a terminal oxidase (“downhill pathway,” indicated in brown text and by **) where they are used to reduce oxygen, or used to reduce NAD+ (“uphill pathway,” indicated red text and by *) in a reaction also driven by the proton motive force across the inner membrane (Bonnefoy and Holmes, 2011). Source: Johnson et al. 2012.


The evidence shows that the tusk is innervated, and acts as a sensory organ to the outside environment, as well as a mating tool.

Sensory ability in the narwhal tooth organ system


You can move it but the parents will likely not return to it or care for the chicks.  If they are nearly ready to leave the nest, perhaps you might wait a bit until that happens.
I'd say put things back the way they were and keep an eye on the nest.  If the parents don't return there is nothing more you can do.


How many cells does the hermaphrodite version of Caenorhabditis elegans have?

959 Somatic Cells according to WormBase and The WormBook.


What triggers the switch between aerobic and anaerobic respiration?

The simplest method of control of metabolism is by substrate concentration. So if the concentration of NADH and pyruvate is low, lactate dehydrogenase cannot function. When they build up it can and will.

The situation is more complicated than this, because pyruvate will only build up if it is not converted to acetyl CoA by the pyruvate dehydrogenase complex (see Berg et al. section 17.1.1):

Although the overall reaction is oxidative, and ultimately requires NAD+, the latter is not directly involved in the initial irreversible reaction. It is presumably for this reason that the reaction is also controlled, either allosterically (in bacteria) or by phosphorylation (in mammals). In either case the regulators are the small molecules the concentration of which is altered by the lack of oxygen: NAD+/NADH and ATP/ADP. The figure below and its legend is also from Berg et al. (section 17.2.1) — available through NCBI Bookshelf.

[The complex is inhibited by its immediate products, NADH and acetyl CoA. The pyruvate dehydrogenase component is also regulated by covalent modification. A specific kinase phosphorylates and inactivates pyruvate dehydrogenase, and a phosphatase actives the dehydrogenase by removing the phosphoryl (group). The kinase and the phosphatase also are highly regulated enzymes.]

The actual situation is quite complex and this is something of a simplification.


How harmless bacteria on skin defence against harmful bacteria?

Relations between organisms in complex ecosystems are various, so I won't give an exhaustive answer, only keys to understanding.

First, you need to consider that a bacterium harmful to humans is not necessary harmul to other bacteria. So there is no reason why our skin microbiota will only target/resist to human pathogens.

What's more, microbes are not inherently harmful to us. Their dangerosity also depends on the capacity of the skin to block them 1.

Then, microbial defence mechanisms depend on the kind of relation they have to the potential pathogen: competition, parasitism, predation, etc.

The article cited below will give you a nice overview on the topic.

1 Cogen, A. L.; Nizet, V.; Gallo, R. L. (2008) Skin microbiota: a source of disease or defence? British journal of dermatology, 158, 3, 442-455; doi: 10.1111/j.1365-2133.2008.08437.x


I would recommend using Biomart from Ensembl. This is basically a Swiss Army Knife for converting gene names into various IDs, getting corresponding locations on the chromosomes and so on. You can upload a list of gene names and convert them into the corresponding gene IDs of other species and the convert these IDs back to gene names.

If you haven't used Biomart yet, you can either start by going on their help page or by having a look on this tutorial for the conversion of IDs.


Why don't plants get hot under sunlight?

Take a look at the Temperature paragraph from this reference:
Ecophysiology

  Plants can avoid overheating by minimising the amount of sunlight absorbed and by enhancing the cooling effects of wind and transpiration.

They seem to have several ways to counter the heat as we do with transpiration, wind etc.

This article is more complicated but as really useful informations on the effects of wind on the plant's temperature:

Leaves in the lowest and highest winds: temperature, force and shape


Why do the size of the phase 1 notch vary among cardiac cells?

Between at least the endocardial and epicardial regions, I believe the transient outward current is facilitated much more in epicardial cells. This article demonstrates the differences in Ito between the two cell types in dogs.

I'm also recommending the following article about Ito phenotypes: "Transient outward potassium current, ‘Ito’, phenotypes
in the mammalian left ventricle: underlying molecular,
cellular and biophysical mechanisms"


Do lizards expand in the summer and contract in the winter?

I think you might be over-extrapolating your knowledge a bit. Animals are mostly made of water, and water only changes density by about 1% between 0C and 37C, so you are overestimating the effects of expansion/contraction due to temperature (and most organisms don't experience such a wide range of core temperatures, outside of special circumstances).

Because water is such an important component of organisms, size would also change with variation in hydration levels (you can easily observe this in plants because many plants use water pressure to support themselves). I would expect this variation to be as great or greater than any expansion/contraction with temperature.

Also note that just because animals are cold-blooded doesn't mean they don't regulate their temperature. Cold-blooded animals move between sun and shade, water and land, etc to regulate their temperature externally.


Where is sialic group in gangliosides that form ABO blood groups?

I suspect this is a product of differentialy expressed glycosyltransferases. Instead of adding a sialic acid, for example, if you're coding for Enzyme B which is an alpha 1-3-galactosyltransferase, you're going to add a Gal to the glycan chain forming B antigen, and so forth. Sialyltransferases can add sialic acid groups, but to the same structure it looks like there is competition between the glycosyltransferases to add sugar moieties that results in different structures getting produced from backbone structures. Source, pages 5-10

  Type-1 units may be modified by glycosyltransferases that transfer sugars to either terminal galactose or subterminal GlcNAc, generating sialylated structures or blood group determinants. The synthesis of type-1 units and expression of the corresponding β1–3 galactosyltransferases are regulated in a tissue-specific manner...

Structures Common to Different Glycans

So that's to say there shouldn't be a sialic acid group on ABO antigens, though sialyltransferases are capable of forming Lewis Antigens (Source). In the anabolic pathway the backbone structure is simply getting attacked by glycosyltransferases and the pathway goes the direction whichever one wins out (level of protein vs level of substrate). Being said, I'm unsure it's proper to say ABO antigens are produced from gangliosides, but if anyone finds some faults in my explanation please let me know!

I'm looking into catabolic pathways that may produce ABO antigens by recycling gangliosides, probably resulting from some cleavages by other glycosyltransferases, I just haven't gotten there yet, I'll try to update if I find anything.


Plants are adapted to the conditions we have here on earth, therefore, for them to grow on the moon we would have to recreate the conditions found on earth (or at least find conditions that we can create and they can grow in). To do this we would need to replicate climate (temperature, air pressure, humidty etc.), provide (sun)light at the necessary intervals and intensity, provide water, air, and nutrients of the right composition, intervals and intensity. That is a simplified version...

In reality there is great variation in how plants require these things. Some cope with long dark periods better than others, some cope with drought better than others, some cope with chemical variation in the soil better than others so answering this question is hard. But generally growing plants on the moon will require the ability to recreate (to some degree depending on the sensitivity of the plant) the conditions a plant has evolved under on earth.

Thus to answer your questions:

Length of day can have strong effects on growth patterns, two weeks of darkness is likely to be a major upset for plants! Just transplanting plants of the same species from different latitudes can affect the growth patterns because of changes in length of day. Try putting some plants in darkness for two weeks and see what happens.

Plants all vary in their ability to meet the requirements of space growth. There will only be a short list of plants that could with "small" modifications to the moon's environment, the more we adapt (adding artificial light, watering, adding nutrients etc) the longer that list would become - the limitation is in our ability to adapt the moon.

See above for reasons why plants might struggle. Oh and we would need to consider the effects of reduced gravity too...

Here's a little something from nasa about how plants are used in space vehicles. And another on light and gravity.


Yes, this is the effect of metabolizing ethanol and also the reason why excess ethanol can lead to hypoglycemia.

Ethanol is oxidized by the alcohol dehydrogenase to acetaldehyde. This reaction consumes one molecule of NAD+ per molecule ethanol oxidized:

Ethanol + NAD+ <=> Acetaldehyde + NADH + H+

Acetaldehyde is oxidized by the acetaldehyde dehydrogenase in a second reaction in the mitochondria to Acetyl-CoA, which produces another molecule of NADH:

Acetaldehyde + NAD+  + CoA <=> Acetyl-CoA + NADH + H+

If you now take a look at gluconeogenesis, there is one critical step which needs NAD+: the oxidation of lactate to pyruvate by the lactate dehydogenase which then cannot be processed into oxalacetate, phosphoenolpyruvate and so on.

Adding excess NADH shifts the reaction equilibrium completely to the side of lactate and also leads to the production of additional lactate, leading to hypoglycemia and lactic acidosis. Excess NADH from the ethanol oxidation inhibits the oxidation of fatty acids in the liver - this process also generates NADH for the production of ATP. NADH signals this process that enough energy is available in the cell. And finally excess NADH also inhibits the malate dehydrogenase reducing the amount of oxalacetate for gluconeogenesis further.


How to get the correct RefSeq Protein transcript for a given RefSeq Nucleotide transcript?

There is another simple way for human sequences.

Go to RefSeq FTP and download the LRG_RefSeqGene file. This file contains updated mappings between the gene, mRNA and protein sequences (latest versions).

From README:

    Tab-delimited file reporting, for each Gene, the accession.version
      of the genomic and RNA and protein RefSeqs the RefSeqGene/LRG
      project treats as reference standards.

    The columns are:
      NCBI taxonomy id (all 9606)
      GeneID
      Symbol of the gene (official from HGNC when available)
      Accession.version of the standard RefSeq
      Term describing the RefSeq
         RefSeqGene              genomic sequence
         Ref Std, nucleotide     RNA sequence
         Ref Std, protein        protein sequence

      The LRG equivalent of the RefSeq standard
         LRG:                    genomic sequence
         t1                      locations for transcript 1
         p1                      CDS from transcript 1

         NOTE: t values can be > 1 ,  the integer assigned to t
               is matched by the integer assigned to p

Some few lines from the file:

9606    3329    HSPD1   NG_008915.1     NM_199440.1     NP_955472.1     reference standard
9606    3329    HSPD1   NG_008915.1     NM_002156.4     NP_002147.2     aligned: Selected
9606    3336    HSPE1   NG_008914.1     NM_002157.2     NP_002148.1     reference standard
9606    3339    HSPG2   NG_016740.1     NM_005529.6     NP_005520.4     reference standard

It is not that easy for other organisms. For them, you should either parse the mRNA page to find the RefSeq protein id or go to their specific designated databases (such as FlyBase for Drosophila) and obtain information on the gene to protein mapping.

For obtaining RefSeq records from NCBI using parsing you should first obtain the GI accession number corresponding to the mRNA.

Example: NM_007393 (mouse beta-actin)

http://eutils.ncbi.nlm.nih.gov/entrez/eutils/esearch.fcgi?db=nucleotide&term=NM_007393

which would give the GI accession number: 930945786.

Then fetch the protein GI using this accession number:

http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=nucleotide&db=protein&id=930945786

which gives the GI accession number: 6671509

Finally get the RefSeq id (if available) corresponding to this GI accession. You can download the feature table and look for the RefSeq i.d:

http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=nucleotide&db=protein&id=930945786&rettype=ft

For more information on how to use Entrez E-Utilities see here.


Black/dark-red smooth West African worm, full of red blood

There are not so many potential candidate worm groups with similar appearance, namely: (free-living) flatworms, Nemertea and annelids.

While there are several terrestrial and freshwater flatworms, some of which are quite long, they do not approach such an elongated vermiform body shape and their mode of locomotion is different. There are around two freshwater nemerteans in Africa, neither of which looks like your worm, and in any case most nemerteans move by gliding using their cilia.

So the remaining group is Annelida. There are three groups of annelids relevant in this context: polychaetes, oligochaetes and leeches. Polychaeta are predominantly marine and normally have more or less pronounced parapodia ("limbs"). Some of the do behave according to your description, but they are very characteristic in their appearance and you would not expect to find them in a bathtub.

What remains are oligochaetes and leeches. Leeches are more or less dorso-ventrally flattened and have very prominent suckers. Moreover a fed leech (from which you would expect large quantities of blood) would look swelled (the gut in leeches has diverticula).

So, the only worm group I can reasonably suggest is oligochetes. In fact your worm looks and behaves very much like a common earthworm. It is very typical of them to be highly mobile during and after rains and their blood pigment is hemoglobin (i.e. red). The only contradiction is that your worm had no clear true segmentation, but I believe, in some forms it is easy to overlook it.

The fly is indeed some species of Psychodidae.


Why do insects (flies) put their legs together when they die (as if they're praying)?

A good working theory is that this is caused by Rigor Mortis and the anatomy of insect legs.

In most cases, the muscles that pull the leg down (or closer together) are larger than the ones that pull the leg up.  This is because those muscles (flexors) must support the insect's weight:

(Click for larger view)

When the muscles contract after death, the larger muscles win out, causing the legs to move together.

From Why Do Insects Cross Their Legs When They Die?:

  I suspect this is rigor mortis -- that post-death stiffening that occurs due to a chemical transformation of muscle tissue -- contracting legs as much as possible in the directions of least resistance, says Brian Farrell, an entomologist at Harvard University.


Is the Insulin Receptor Considered an Enzyme?

Yes, the insulin receptor can be viewed as an enzyme, since it catalyzes a reaction -- phosphorylation of tyrosine residues on its substrates. But since the protein has multiple functions, it's probably better to say that the insulin receptor "has enzymatic activity", rather than "is an enzyme".

The notion "enzyme" is not restricted to catalysis of reactions involving small molecules, like those in central metabolism. The IUPAC definition of an enzyme reads: "Macromolecules, mostly of protein nature, that function as (bio)catalysts by increasing the reaction rates". So "enzyme" is a broad term, including catalysis of all chemical reactions. DNA replication, mRNA transcription, protein synthesis and posttranslational modifications all involve enzymes. Those enzymes that act on small metabolites can be called "metabolic enzymes" to clarify their function.


Method to recognize the age of a firebug from the pattern on its back

The answer is more or less yes. Normally Firebugs (Pyrrhocoris apterus) go through 5 nymph instar stages (as do most Hemiptera), where they resemble the adults more and more as they grow. Only adults are winged and have have functional reproductive organs. This type of metamorphosis is called hemimetabolous or simple metamorphosis (in contrast to Holometabolism or complete metamorphosis). However, I cannot find a good overview of the instar stages of Firebugs to link to.

A generic overview of Heteroptera (True Bugs) can bee seen here
(from www.amnh.org/learn/biodiversity_counts):

This picture shows (at least) three instars + adults of Pyrrhocoris apterus (from http://www.projectnoah.org/spottings/17248017). The large nymph with 3 dots along the midline is the final 5th instar nymph:

However, due to hormonal disruptions there have been cases with even more nymph stages (6th and 7th instars with adult characteristics), but this is under unnatural laboratory conditions (e.g. Slama & Williams 1965 and Konopova et al. 2011). Konopova et al (2011) also has pictures of instar stages 4 & 5 (along with gene knowdown versions).


What is this green micro-organism found living in water?

I can't decide if it's a eukaryote or a prokaryote.

Well, that's certainly an eukaryote. We can clearly see the nuclei in the cells of your fist picture, as well as in the cells of your second one (not so clearly, though):

In the image above, the arrow starts right on one of the nucleus of that group of (apparently) three cells.

Besides that, despite some cyanobacteria being very long, 10µm is a lot for a prokaryote. The mean size of cyanobacteria is way less than that.

By the way, this:

  ... a prokaryote or a cyanobacteria (that can combine both characteristics)

Doesn't make much sense, because cyanobacteria are prokaryotes. More precisely, they are Eubacteria prokaryotes.

Finally, what eukaryoyte is this? I can't tell. It's most probably a kind of Chlorophyta, but I'm not able to go to the Class level. If you're interested in identifying it, you can try a taxonomic key. This one is for British freshwater algal flora, I don't know how different French algae are from the british ones: The Freshwater Algal Flora of the British Isles: An Identification Guide to Freshwater and Terrestrial Algae.

If I'd guess (and this is a wild guess), I'd say that this is a Chlorellales, as the famous Chlorella:

Also, have in mind that saying "that's an alga" doesn't help as well: worse than paraphyletic, algae  is a polyphyletic group and, in biology, polyphyletic groups mean almost nothing.


After a lot of scrolling through image searches I stumbled upon the answer: this is the egg mass of some sort of horse-fly (Tabanidae). Almost identical egg mass here: http://bugguide.net/node/view/21171

I'm assuming I won't get a more specific answer than this.


Is it possible there were multiple origins of life? And, if so, why did the one which became the common ancestor between all organisms prevail?

It is interesting that all forms of life use the same genetic code. The nucleotides composing DNA and RNA are universal. Eric Lander, geneticist from Harvard/MIT cites this as evidence for evolution from a single ancestor. I think your instructor may be saying that it's possible alternative adaptations for initiation of life may have occured and perhaps not worked out. They become just another of nature's experiments that ended in extinction. I seem to recall reading somewhere all but 2% of species have ended in extinction.


Question about the Derivation of the cable equation for neurites

The part you are quoting is about helping you conceptualize the cable equation by starting from some approximations that let you remove most of the terms. See the sentence beginning (emphasis mine):

  To better understand how the cable equation is derived, first simplify the theoretical neuron even further and pretend...

They then walk you through how, because these approximations are just pretend, one needs to include terms to account for the actual permeability and capacitance of the membrane. This means that you do not have a constant internal current with distance as you travel along; instead, the current decays with distance because of leak through the membrane and membrane capacitance.

This is what the last equation you quote from says: the change in internal current over distance x (written as dil/dx) is equal to the current lost to the membrane, which includes two parts: leak through the membrane (V/rm) and charging the membrane capacitor (cm*dV/dt).

Another correction that might be tripping you up: you write

  change in voltage over time

in your question, but that is not what the equations are representing, they are representing change in voltage over distance x.


There are two pieces to this question:

a) How does bone resorption (movement of Ca/Phos out of bone into the blood) result in net improvement in bone structure?

Bones are constantly remodeling, primarily in response to mechanical stressors. Although you clearly already realize this, I will make it explicit: osteoblasts are the cells that create new bone; osteoclasts break down (resorb) bone.

Quoting Harrison’s Internal Medicine1:

  Radioisotope studies indicate that as much as 18% of the total skeletal calcium is deposited and removed each year. Thus, bone is an active metabolizing tissue.…The cycle of bone resorption and formation is a highly orchestrated process carried out by the basic multicellular unit, which is composed of a group of osteoclasts and osteoblasts

Bone mineral density (BMD) can not be equated with bone quality. (This is the difference between osteoporosis – deficient bone density – and rickets – poor bone architecture.) Thus, vitamin D’s stimulation of both osteoblast and osteoclast activity is beneficial to bone structure.

b) How does vitamin D lead to overall increased bone density?

In addition to the effects above, you mentioned that vitamin D increases serum calcium by several mechanisms. This is true. Both this increased serum calcium as well as the direct effects of Vitamin D on the parathyroid gland suppress PTH production.* As PTH has powerful actions to increase bone resorption by mobilizing calcium and phosphorus to move from the bone into the blood, the suppression on its excretion applied both directly and indirectly by Vitamin D results in a net increase in bone density.

Thus, both by its effects on bone quality and quantity, vitamin D is a net boon for the bones.

*Parathyroid hormone, a.k.a. parathormone. There is a paradox here, because drugs such as teriparatide (a.k.a. Forteo, recombinant PTH) are anabolic for bone and are used to treat osteoporosis. Although the mechanism is unresolved, intermittent administration (as in the case of drug treatment) increases BMD while chronic sustained elevations decrease BMD.2

References

1. Bringhurst F, Demay M.B., Krane S.M., Kronenberg H.M. (2012). Chapter 352. Bone and Mineral Metabolism in Health and Disease. In Longo D.L., Fauci A.S., Kasper D.L., Hauser S.L., Jameson J, Loscalzo J (Eds), Harrison's Principles of Internal Medicine, 18e.

2. Rosen CJ. The cellular and clinical parameters of anabolic therapy for osteoporosis. Crit Rev Eukaryot Gene Expr. 2003;13(1):25.


Why is pollen used as a dietary supplement?

Bee pollen contains high concentrations of reducing sugars, essential amino acids and unsaturated/saturated fatty acids. It contains minerals such as Zn, Cu, Fe, and high K/Na ratio and significant quantities of several vitamins. Note that the composition of it varies greatly depending on their botanical type and the techniques used by industries. It is basically the collection of pollen grains from flowers made by worker honey bees with nectar and salivary substances.[Source 1](Page 1)  [Source 2]

[Source 1](Page 4)
The claimed benefits of bee pollen are based on biological and therapeutic activities. The main components are phenolic acid derivatives and polyphenolic compounds. They are known to possess properties such as anti-oxidant, anti-aging, anti-carcinogen, anti-inflammatory, anti-atherosclerosis, cardio-protective and improved endothelial functions. However, it is unknown that treatments with such products are effective or not and how to minimise the health risks.[Source 1](Page 5) [Source 4]  [Source 5]  [Source 6]
Different studies were conducted in mice on the nutritional effects of bee pollen. It improved food digestion and also improved reproduction rates. Chickens fed with bee pollen had a better development of the small intestine. This suggested that bee pollen helped in early development of the digestive system. Bee pollen is also taken as a supplementation by athletes for improvement of performance. Controlled experiments indicated that no positive benefits were obtained. However, the number of training missed due to respiratory tract infection was lower in the bee pollen treated group.[Source 1](Page 5)

Pollen digestion:
Doubts have been raised, whether the tough shell of pollen can be breached and digested by humans. It was discovered in animal experiments that pollen did not retain its content after leaving thedigestive tract. This gave rise to the hypothesis that the nutritional content of pollen was released by the digestive juices in animals (Schmidt & Schmidt, 1984; Roulston & Cane, 2000). In humans it was once shown that pollen was absorbed in the digestive tract (Jorde & Linskens, 1974) or that it was partly digested, (Franchi et al., 1997) whereas there were differences in the degree of digestion of poppy and hazelnut pollen, with an average degree of digestibility of 15% for carbohydrates and 53% for proteins.
In this case it has been hypothesized that pollen was insufficiently digested and that cracking would improve the digestibility and bioavailability (Rimpler, 2003). Different companies offer cracked bee pollen, claiming that this product is better digested. On the other hand, there are many studies in humans with whole bee pollen showing that a part of the bee pollen content is digested and is bioavailable. However maceration of pollen for several hours in water or other liquids is recommended in order to improve digestibility, this method is used also for other heavy digestible grain products.[Source 1](Page 3 & 4)

Flower pollen:
Non-bee pollen are called flower pollen. Extensive health relevant research has been conducted on pollen prepartions from non-bee pollen. It is marketed under names such as Cernitron, Cernitol, etc. It is known to decrease prostrate hyperteophy in rats, but there was no relevant changes in blood levels of LH, FSH, testosterone or dihydro-testosterone.

In patients with prostatic adenoma the improvement was in nycturie, important decreases in the residue post-urinate and in long term treatment, also decrease in the diameter antero-posterior of prostate. The urinary debit did not suffer any changes. The effect on the other symptoms usual in the hyperthrophie benign of prostate was not of statistical significance (Bruneton, 1999).[Source 1](Page 7)

For industrial benefit:

Improved bioavailability is important in the pharmaceutical industry in that it reduces costs and increases the effectiveness of drugs. Previous studies have shown that this enhancement is possible using exines from pollens and plant spores. In one example the ingestion of ethyl ester derivative of EPA (eicosapentaenoic acid) encapsulated in sporopollenin microcapsules from L. clavatum spores improved the bioavailability of EPA in the bloodstream. In these trials, six volunteers ingested 4.6 g of fish oil containing 20% of the EPA ester, both alone, and encapsulated, as a 50% fat content powder, respectively. The bioavailability of the active was defined by area under curve (AUC (area under curve) 0–24 h). The mean AUC 0–24 of EPA from ethyl ester with exine was remarkably 10-fold higher than the corresponding for ethyl ester without exine encapsulation.
In other unpublished studies involving human volunteers, ingesting a lipophilic active, the enhancement of bioavailability has been very similar. The mechanism by which such enhanced bioavailability is achieved is intriguing and some preliminary experiments have been undertaken to explore possible explanations. Recent in vitro studies (unpublished studies) revealed that the exine shells exhibited gut mucosal adhesion properties. In addition, in vivo experiments on mouse microtone sections of intestinal walls of mice fed with exines showed the exines to lie between the gut villi. The unique morphology of exine shell surfaces probably evolved to help pollen particles to become attached to insects and thereby aid the process of pollination. It is possible therefore that this same morphology could help the exine’s adherence to and close association with the gut wall leading to an increase in the period of contact between the encapsulated drug and the biological surface, thereby enhancing its absorption and bioavailability.[Source 3]

Hazardous components of pollen:

Trace amounts of hepatotoxic pyrrolizidine alkaloids were found in pollen of Echium vulgare, E. plantagineum, Senecio jacobaea, S. ovatus, and Eupatorium cannabinum (Boppre et al., 2008).  In Middle and Northern Europe these pollens are not among the main pollen grains gathered by bees, however in Southern Europe the two Echium plants are more  diffused and are gathered by bees in larger amounts (Campos et al., 1994; Serra Bonvehi, 1997). [Source 1] (Page 5)

Therefore, it should undergo tests to approve it's purity as allergies can be caused.
References:
1 : Future of bee pollen(Research gate)
2 : Pollen composition and standardisation of analytical methods(Research gate)
3 : Hollow pollen shells to enhance drug delivery(NCBI)
4 : Bee pollen: chemical composition and therapeutic application(NCBI)
5 : Biological activities of commercial bee pollens: antimicrobial, antimutagenic, antioxidant and anti-inflammatory(NCBI)
6 : Biological and therapeutic properties of bee pollen: a review(NCBI)


How common are the "common" human coronaviruses?

The common [cold] coronaviruses are pretty common:

Four HCoVs (HCoV 229E, NL63, OC43, and HKU1) are endemic globally and account for 10% to 30% of upper respiratory tract infections in adults.

To pick a more detailed study in Ghana:

This study sought to determine whether human coronaviruses (HCoVs) are associated with upper respiratory tract infections among older children and adults in Ghana. We conducted a case control study among older children and adults in three rural areas of Ghana using asymptomatic subjects as controls. [...]
Out of 1,213 subjects recruited, 150 (12.4%) were positive for one or more viruses. Of these, single virus detections occurred in 146 subjects (12.0%) and multiple detections occurred in 4 (0.3%). Compared with control subjects, infections with HCoV-229E (OR = 5.15, 95%CI = 2.24–11.78), HCoV-OC43 (OR = 6.16, 95%CI = 1.77–21.65) and combine HCoVs (OR = 2.36, 95%CI = 1.5 = 3.72) were associated with upper respiratory tract infections. HCoVs were found to be seasonally dependent with significant detections in the harmattan season (mainly HCoV-229E) and wet season (mainly HCoV-NL63).

Occasionally there are substantial outbreaks of common cold, e.g. as observed in Japan:

we conducted a longitudinal survey
between 2010 and 2013 in Yamagata, Japan, to clarify
the epidemiology of HCoVs using RT-PCR methods
[...]. In 2011, we
found that the monthly detection frequencies of HCoVNL63 were higher than 20% in January and February
(28.5% and 25.3%, respectively), whereas those of the
other HCoVs (HCoV-229E, -OC43, -HKU1) did not exceed 20%. In light of these findings, we continued
the HCoV surveillance and, thus, captured data from
the largest outbreak of HCoV-OC43 reported in the last
6 years. During the 2014–2015 influenza season in
Yamagata, Japan, the monthly detection frequencies
were approximately 30–40%.

Those percentages are from people reporting symptoms (and then swabbed.) The graph below (from the same paper) nicely shows the seasonality.

Monthly distribution of clinical specimens (A) and HCoVs (B) detected from patients with acute respiratory
infections between January 2014 and March 2015, in Yamagata, Japan.

Question 2 is rather meaningless because immunity to common coronaviruses is short lived. See (also) this answer (esp. the 2nd table) to a related question putting the common coronaviruses immunity duration in perspective; reproducing just the table below (the relevant line for common coronavirus is the 1st below the break, i.e. 1st in the 2nd section of the table).

And I've managed to track down one of the primary studies on 229E long-term immunity (or rather lack thereof)

Although after 1 year concentrations of specific serum IgG and nasal IgA were
still significantly raised in the infected group, they were much lower than at the
maximum. [...] When challenged after 1 year all of the original uninfected group were infected and 6/9 of the infected group were reinfected. [...] In the infected group there were considerable individual differences. Some lost their antibody, particularly serum antibody, completely by 1 year, some did not.

And it's basically impossible not be exposed to a strain of the common cold coronaviruses at one point; one study on newborns found that interval to be 3.5 years, but that's probably an overestimation for adults.

all of the children had maternal anti-NL63 and anti-229E antibodies at birth that disappeared within 3 months [...] on average, HCoV-NL63 and HCoV-229E seroconversion occurs before children reach the age of 3.5 years.

The real question is whether Covid-19 will behave like the common coronaviruses or more like SARS and MERS for which it is suspected (from the detection of antibodies), but not certain that immunity lasts longer.

For the SARS and MERS coronaviruses, antibodies appear to persist for several years, but no studies have intentionally attempted to re-infect people, since these are deadly diseases.


Will new proteins incorporating new amino acids trigger an immune response?

Introduction

This question has two components. The first is the near rhetorical question whether proteins with unnatural amino acids will be considered by the immune system as ‘non-self’. Unless, by chance, the unnatural amino acid resembles some normal macromolecular component, the answer is obviously that it will be regarded as ‘non-self’.

The second question is, to my mind, much more interesting, but does not appear to be considered (or has been taken for granted) in the answer by @Astrolamb. This is whether the immune response would cause such artificial proteins to be eliminated, if  administered therapeutically. It is important, at this juncture, to emphasize that proteins containing unnatural amino acids as the result of expanding the genetic code do not, in principle, raise any problems of immune ‘rejection’ that have not already been seen in ‘unnatural’ proteins containing normal amino acids. Any immune response should therefore be regarded as being to ‘non-self protein’ and rather than to ‘non-self amino acid’.

As there have been many such studies with the latter proteins (and with proteins containing unnatural amino acids introduced by chemical modification) there are extensive studies on which to base an answer. An immunologist would be a better person to do this, but in the absence of any “immune response” I will attempt an answer from my perusal of the literature, leaning particularly on:

K. Wals and H. Ovaa “Unnatural amino acid incorporation in E. coli: current and future applications in the design of therapeutic proteins” Front. Chem 2, 1–12 (2014)

and

B. Leader  et al. “Protein therapeutics: a summary and pharmacological classification” Nature Reviews Drug Discovery 7, 21–39 (2008)

I welcome comments suggesting improvements or corrections.

Summary

The question asks:

  “if new proteins are made from amino acids that don’t naturally occur,
  won’t the body reject them?”

which I take to mean:

  “if new proteins are made from amino acids that don’t naturally occur,
  won’t they induce an immune response which will render them
  ineffective?”

The brief answer to this is:

It depends — the immunogenicity of foreign proteins varies.
Even if an immune response is elicited this may not necessarily render such proteins ineffective.
In some cases the therapeutic intention is actually to provoke an immune response — to make a weakly immunogenic protein more so.

Foreign proteins vary in immunogenicity

The crux of the answer to this question lies in the following:

  The fact that a protein used for therapeutic purposes differs from
  those in a human subject does not in itself mean that it will invoke
  an immune response.

Let us consider two examples to illustrate this.

The first is the case of porcine insulin, which has been administered to patients for many years, but has one amino acid different from human insulin. Regarding such non-human insulin this review states that “severe immunological complications occur rarely, and less severe events affect a small minority of patients”.

The second example is taken from more recent work by D-A. Silva et al. in designing artificial proteins. (See also Nature News & Views summary). They designed mimics of the cytokines, interleukin-2 and interleukin-5, that had extensive differences in helix organization and amino acid sequence from the native proteins. However they reported that “Immunogenicity against the de novo designed proteins appears to be low”.

It turns out that  a wide variety of factors affect the immunogenicity of foreign macromolecules, so that even if a therapeutic protein elicits an immune response it may be weak enough to allow the therapeutic action to occur. In the work just cited, Silva et al. suggest that the reason for the low immunogenicity might be “the small size and high stability” of the proteins on the basis of previous work they had performed with 20,000 mini-proteins.

Admittedly, in some cases a strong immune response will occur and can obviously be a problem, so that measures need to be taken to reduce the immunogenicity. This is widely recognized and discussed in the following paper:

V. Brinks et al. “Immunogenicity of Therapeutic Proteins: The Use of Animal Models” Pharm Res (2011) 28:2379–2385

Sometimes chemical modification of proteins can actually reduce their immunogenicity, as is the case for polyethylene glycol in relation to interferon (B. Leader et al. review, cited above).

Use of therapeutic proteins to provoke an immune response

One use envisaged for modified proteins is in cancer immunotherapy. In brief, the objective is to try to make the body mount an immune response against cancer cells, which may exhibit ‘foreign’ tumour antigens. However, in many cases these differences from normal cells are not sufficient to provoke an adequate immune response. It is has been shown that modifying retinol binding protein by introducing an unnatural amino acid can help overcome the self-tolerance to tumours in mice, suggesting a possible use in cancer immunotherapy  (J. Grünewald et al. “Mechanistic studies of the immunochemical termination of self-tolerance with unnatural amino acids” PNAS (2009) 106, 4337–4342).

Conclusion

Proteins containing unnatural amino acids as the result of expanding the genetic code do not, in principle, raise any problems of immune ‘rejection’ that have not already been seen in ‘unnatural’ proteins containing normal amino acids or chemically modified amino acids. The problem of potential immunogenicity is widely recognized and has been extensively studied by those wishing to develop the considerable therapeutic potential of all such proteins.


Why does it hurt more when you touch a nerve directly?

I answered the other question and it is similar. However, this one is different enough that I will give a slightly more simple explanation.

Nerves transmit messages using electrical current, more specifically the flow of sodium and potassium. Just remember that it's electricity. When you have any sort of cut or damage, your body recruits white blood cells which protect you from any bacteria that might enter. They also cause inflammation to prevent those bacteria from spreading (and to warn other cells that they may become infected). It is also important that we feel pain, so we know something is wrong (because we have the ability to do something about it). That's why inflammation causes pain. It does this by lowering our threshold so our nerves are more sensitive. In other words, it takes less damage, pressure etc. to cause our nerves to send the pain signal. Normally, it is set higher, so we don't suffer too much pain. Naturally if you want clarification on anything just ask.


One key nutrient worth thinking about in the context of this question is vitamin B12. Herbivores such as cows and sheep will derive this directly from the bacteria in their rumen. Rabbits produce two types of feces - soft and hard - and they eat the soft variety, rich in gut bacteria, as a source of nutrients like vitamin B12. Gorillas are primarily herbivores, but are thought to derive their vitamin B12 from insects, eaten purposefully or inadvertently.

So yes, herbivores derive this particular nutrient from non-plant sources.


Looks like a mountain beaver (Aplodontia rufa) to me. Location, appearance, and minimal tail all match.

A bit more detail:

Where I'm from on Washington's Olympic Peninsula, they're not uncommon, but Butte County is near the southern end of their distribution (eol map page) and they may be less common there, and limited to cooler higher elevations (Beier 1989), and to wet habitats (their inability to concentrate urine (!) means they need to drink enormous quantities of water).

This white paper from USDA (Arjo 2007) is a great source, and more comprehensive than the  the wikipedia page, which is also good.

Arjo, Wendy M. (2007). "Mountain Beaver: A Primitive Fossorial Rodent". USDA National Wildlife Research Center - Staff Publications. Paper 675.

Beir, Paul (1989). Journal of Wildlife Management 53(3) 649-654


What is the evolutionary advantage of menstruation?

Human female ovaries only have a certain number of ova; none are manufactured in adulthood. Once they're gone (that's when menopause occurs), they're gone.

You can also ask, why did evolution result in a limited number of oocytes then? This kind of second guessing of physiology is endless.

In your scenario, an ovum would need to be released every few days in order to be fertile continuously. That alone would decrease the number of years that a woman could be fertile. Since a fetus needs about nine months to gestate, I think once a month fertility is more than adequate. The earth's population is already too large, which also translates as successful reproductively.

If a fetus could gestate in a month, I could see an advantage to constant fertility. But the disadvantages would also be great. How could a woman take care of so many babies? How could she possibly feed, say, six to nine babies a year with only two breasts? (Mammals that frequently have larger litters have more mammary glands.) How could her own body compensate nutritionally not only for the burden of feeding the fetuses but also of the babies?

Asking why didn't something evolve from a teleological standpoint rarely results in a satisfying answer. If constant fertility were advantageous, maybe it would be present.


Why does the affinity of haemoglobin for oxygen increase at higher elevations?

The question seems to be based on the idea that there would be physiological adaptation to low oxygen, possibly through the Bohr effect. In fact the usual mechanism of adaptation is through genetic change.

There are a lot of examples of animals which live (or fly) at high altitude and which have a haemoglobin with a higher oxygen affinity. Examples which spring to mind are the bar-headed goose and the camelids of South America (llamas, alpacas etc.)

Haemoglobin has evolved as an efficient oxygen-delivery protein by having a variable affinity for oxygen: low affinity at low oxygen concentration, high affinity at high oxygen concentration. This is achieved through co-operative binding (allostery), and it ensures that the protein loads up with oxygen in the pulmonary circulation but releases oxygen in the peripheral tissues.

At high altitude, where the partial pressure of oxygen is lower, the haemoglobin of humans, for example, will not be fully saturated, impairing the delivery of oxygen to the body. Haemoglobin variants with an increase in the overall affinity for oxygen can achieve full loading at the expense of slightly less release in the tissues - overall a better oxygen delivery function. This is what happens in the camelids, but there is no such adaptation in humans living at high altitudes.


I am not sure I understood your question. I will try to rewrite your question below with my own words and you will let me know if I udnerstood your question correctly.

Description of the genetic of interest

There is only one locus for coat color. Individuals are diploid. At this locus, there exists 4 alleles in the population. B, R, Y and W. BR individuals are both black and red (as B and R are codominant). Another individual is YW and its phenotype is yellow and white (as W and Y are codominant)

Question

What phenotype do BY, BW, RY and RW have?

Answer

There is no way to know! Relationships between alleles, say Y and B in determining a given phenotype cannot be extrapolated from relationship B and Y have with other alleles. A relationship between two alleles in determining a phenotype is specific to a pair of alleles.

It is for example theoretically possible that A is dominant over B and B is dominant over C and C is dominant over A.

In your case, as you only have codominant relationship, it is tempting to expect that BY would be both black and yellow but there is really no way to be sure of that from the "Description of the genetic of interest"

EDIT

You have now changed your post. I don't really understand the new question either. You seem to imply that two alleles may be both dominant. This is impossible. They can be co-dominant.

I think your issue is that you are trying to associate a property of relationship between alleles as a property of an allele itself. Keep in mind, that saying that an allele is dominant only makes sense in a particular context that is in relationship to another allele who will therefore necessarily be recessive.


What is this insect in a cocoon climbing a web?

That is, probable, a Psychidae (Lepidoptera), commonly known as bagworms. They build those "bags" with pieces of wood, twigs and leaves, and they protect them from predators and parasitoids. One possible species for Florida is this one: https://en.wikipedia.org/wiki/Evergreen_bagworm


Generalism - specialism index in microbial ecology

I've published a paper comparing different measures of specificity, if that is of any help. But if you plan to have, e.g., measures of performance on carbon sources, pH, and temperature, then you'll have three measures of specificity (i.e. one for each).

Also, worth to have a look at Graham Bell's inconsistency and responsiveness, as used by Venail et al. to classify specialists and generalists.


Neuroendocrinal mechanism of parturition

These hormones are progesterone and estrogens. They are actually secreted by the placenta, in increasing amounts as the fetus matures:

(Colorado State, R. Bowen)

You can see that the placenta produces both types of hormone in increasing amounts until birth. Additionally, the hormone relaxin is secreted by the placenta and thought to aid in parturation:

  Relaxin is a hormone thought to act synergistically with progesterone to maintain pregnancy. It also causes relaxation of pelvic ligaments at the end of gestation and may therefore aid in parturation. In some of the species in which relaxin is known to be produced, it is produced by the placenta, while in others, the major source is the corpus luteum. In some species, relaxin is produced by both the corpus luteum and placenta. - R. Bowen


Is Urea excretion a shared ancestral trait of amphibians and mammals relative to synapomorphic Uric Acid excretion in living reptiles?

There are reptiles that also use urea, and mammals that excrete uric acid.  it is likely that urea is the ancestral condition (compared to uric acid) as it occurs in adult amphibians and some fish. But ammonia is even more ancestral than that, occurring in young amphibians and most fish. It is likely uric acid developed alongside terrestrial eggs, as every egg laying amniote (including monotremes) uses uric acid at least during the embryonic stages. Uric acid is more metabolically costly so there is some incentive to switch to urea if you can, although there is a counter factor as urea requires significantly more water. so it comes down to which a group can afford more water or calories. It is notable that the few reptile to witch use urea only switch during their adult stage. It is possible to do both a few desert mammals produce uric acid and urea at the same time, producing more uric acid when water stressed.