What evidence do we have to derive a rate of evolution?

This question is very broad. And because of its broadness, I am afraid you won't find a database that will give you what you're looking for.

Are you interested in some specific phenotypic traits?
Or in some specific genes?
What time scale are you interested in?
Do you want to know about the time that a given allele needed to reach fixation?
Do you want to compare the number of mutations that accumulated in a given DNA sequence between human and close relatives (apes, primates, mammals, ..)?
Do you want to compare the evolution of the mitochondrial DNA between human populations that have different mating systems?
Evolution in response to HIV?

If there is one specific gene or trait (including traits such as the mutation rate) that interest you, you might want to ask a more specific question on another post.

Concerning the methodology, I agree with shigeta that probably the main methodology you'd be interested in is molecular clock. The ratio of synonymous over non-synonymous mutations are also of interest to compare rates of evolution. Comparisons of mutations accumulation between different sequences. But you might also be interested in fossil records (depending on the trait and the time scale you're interested in). Or more interestingly in selective sweeps. Selective sweep is the reduction in polymorphism and heterozygosity of linked loci to the locus under selection. In humans examples exist in the microcephalin gene or in the lactase gene for example. You might also be interested into allele frequency cline over spatial distribution and things like that. Comparison of evolutionary rates between populations of different size might also give you some insights in how quick does evolution occurs in humans. There are probably tons of other methodologies one could use.

You talk about comparisons between empirical data and theoretical model. But again the question is too broad I think. There a tons of different models to be considered depending on what you are interested in.


What are the major evolutionary pressures for Bioluminescence?

In many cases, and in particular in marine invertebrates, the bioluminescence is in fact produced by symbiotic bacteria of the Vibrionaceae family. In most cases the bacteria can sense when they are being hosted by the animal through quorum sensing mechanisms, and start producing light.

The evolutionary pressure for the bacteria to produce light is to be in the protected environment of the animal which often feeds them. On the animal side, there can be several reasons to host the luminescent bacteria. In many cases, the evolutionary pressure is linked to reproduction. In order to successfully reproduce in the immensity of oceans, marine animals need to know that they are among their kind before they release their gametes.

Another example is the one of some deep see fish like the anglerfish which have developed a special "flash light" organ to host bio-luminescent bacteria. Fish can use the bacteria to emit a light to aid in camouflage, hunting, and attracting mates. See http://microbewiki.kenyon.edu/index.php/Deep_sea_fish


Is the leading strand consistent in the same chromosome with multiple replication forks?

Replication proceeds in both directions from a single origin of replication, so the same strand acts as both the leading or lagging strand for the two different replication forks.


What do we use as baseline to determine what genetic segments are "mutations" (and what are not)

It may help to think about the genealogy of the sequences in question. In general, we suppose that all DNA sequences from organisms are related by a set of processes. A particularly important process relating DNA sequences is replication. This establishes a parent-child relationship between DNA sequences in one round of replication or an ancestor-descendent relationship when we view more than one round of replication.

For simplicity, consider a single bacterial cell, which replicates its genome and divides, yielding a descendent cell. This process continues for each cell and produces a population of cells over time. This population of cells (and their genomes) are related to each other by this process of replication and division. The structure of this relationship is a tree (in the mathematical sense). The vertices of the tree are the DNA sequences (or cells) and a directed edge from vertex i to vertex j exists if and only if the sequence represented by vertex j is the result of a replication of the sequence represented by vertex i.

In addition to the replication process which makes this tree structure relating sequences, there are mutational processes that lead to sequence differences.

There are many ways for mutations to arise before or during DNA replication. The important thing to note is that these mutations are passed on to descendants. So, a cell is either genetically identical to its parent cell, or it contains some number of mutations (insertions, deletions, or polymorphisms in the DNA) with respect to its parent.

These mutations (sequence differences) are inherited during replication, and you can think of them as "occurring" along a given edge in the tree from a parent cell to a child cell.

Now, if you consider any two DNA sequences, as well as the model just given, these two sequences are related through the replication-mutation process (the tree). If the DNA sequences are not identical, you have many ways to interpret this question of what is a mutation. It is useful to consider the most recent common ancestor of the two DNA sequences in making sense of the differences observed in the DNA. If you think of the genealogy as a tree, and you're considering two vertices in the tree, then tracing backwards towards the root of the tree from each vertex, these traces will eventually meet at another vertex. The first vertex at which they meet is the most recent common ancestor.

It is possible that mutations have occurred along both paths from the (most recent) common ancestor to the descendent sequences you're investigating. If you're investigating N sequences, there are N paths from the common ancestor on which mutations may have occurred.

All of this is to say that mutations occur with respect to this genealogical process. If you just consider 2, or N, sequences without regard to the process that generated them, then it can be meaningless or confusing to consider a particular sequence difference as a mutation with respect to another sequence under consideration. For example, if you observe a single nucleotide polymorphism between two sequences, how would you know which sequence was the result of the mutation? It is possible that one or both sequences carries a mutation event in its genealogical history since the common ancestor of both sequences.


How can soft tissue exist in dinosaur fossils?

keratin and collagen are an incredibly tough molecules so if it is isolated from the environment (oxygen and bacteria) it could easily survive for that long. Not all proteins are equal some are very robust other very fragile. We have long known protein and carbohydrates can survive for incredible lengths of time under the right circumstances, amber is famous for it. Rapid deposition of minerals can produce a similar if less powerful result.

In this case the keratin was encapsulated by water deposited minerals that sealed it away from the outside environment. There are other examples as well, natural mummification can lead to some preservation in the form of biofilms and impressions. But the most dramatic are amber encased specimens. Amber is a quick forming and creates a perfect air seal.

here is a dinosaur tail preserved in amber.


How much time do INS1-E and MIN6 cells need after splitting?

Searching literature to see what the published protocols were is the best bet. I found a simple document for INS-1 cells here. There is also this paper describing the isolation of an Ins-1-derived cell line 832/13 which my lab (though not me personally) have experience with. Cells should only be sub-cultured when nearly or fully confluent. With Ins-1 cells that would be a sub-culture ratio of 1:4 to 1:8 and will take 2-3 days. Something to note is that Ins-1 cells are poorly adherent to tissue culture plastic. That's a normal part of their characterization. I remember lab members having to take special precautions with respect to media ingredients to prevent them from detaching, as well as really delicately adding media to the dishes otherwise the force from pipetting too quickly will dislodge many cells and explain why your cells are washing away.


How can one calculate "probability of possessing a ‘perfect’ profile" from "typical optimal genotype frequencies"?

They appear to have simply considered each allele independently. This means that if there are say 2 alleles for a trait, and they are both present at a frequency of 0.1 in the population, then you have a 0.01 chance of having both of them. This is probably an okay assumption for their purposes (in reality some might be linked and would associate non independently). Their point is simply that as the number of alleles go up, having all the best ones becomes increasingly unlikely.


Why does inversion happen? What is its purpose?

Like many other mutations, inversion is generally a neutral mutation. Many inversions, especially those which are between small, intergenic regions, evolve neutrally by drift alone. However, selection can, and does, occur when:

inverions create structural problems with meiosis, like pericentric inversions
a breakpoint disrupts open reading frame or alters gene expression
inversion carries one or more selected alleles

Thus, inversion does not necessarily yield any advantage, but it usually does not cause any harm either (Kirkpatrick, 2010).

  Can chromosome inversion fall under harmful mutation.

No mutation is useful or harmful by default. It depends on what effect it gives in every case. Similar is the case with chromosome inversion. It is mostly a nuetral mutation, occasionally harmful, and rarely useful for the individual. Thus, in a way, it can be classified as a neutral mutation.

  What is so important about centromere?

The main point to ponder is how the two types of inversion affect daughter cells, especially during meiosis. For introduction, in a paracentric inversion, the centromere is not involved, while it is in pericentric inversion.

Now consider paracentric inversion during meiosis. Start with a diagram:

Due to a paracentric inversion during a crossover, formation of a dicentric bridge and an acentric fragment takes place. While the acentric fragment, due to lack of a centromere, is lost from the genome, the dicentric bridge forms such structure that the two remaining chromatins lie farthest apart. Eventually, due to tension, the homologous chromosomes break apart, leading to formation of chromosomes lacking certain genes. This makes the gamete and/or the zygote inviable, and reduces the recombination frequency.

Now, while very similar thing happens in pericentric inversion, the mechanism is a bit different. Again, see the diagram first:

Since the centromere is also involved in inversion, the genes on both arms of chromosomes are, as a result, inverted. When crossover takes place, both homologous chromosomes receive two copies of one fragment and no copies of the other. As a result, again, the gamete and/or zygote is inviable and the recombinant frequency is reduced (Griffiths et al, 2000).

  When does chromosome inversion happen?

Just like all other mutations, chromosome inversion can occur at any stage of life in an individual. It is not limited to meiosis, it can occur in any replicating cell in the body. However, the phenotypic effects are most prevelant when it occurs during meiosis, since it can easily lead to defected or inviable progeny.

References:

Kirkpatrick M (2010) How and Why Chromosome Inversions Evolve. PLoS Biol 8(9): e1000501. doi:10.1371/journal.pbio.1000501
Griffiths AJF, Miller JH, Suzuki DT, et al. An Introduction to Genetic Analysis. 7th edition. New York: W. H. Freeman; 2000. Inversions. Available from: https://www.ncbi.nlm.nih.gov/books/NBK22042/


centiMorgan distribution among human chromosomes

The short answer is "yes". Here is an early example: https://science.sciencemag.org/content/265/5181/2049.abstract

I am sure that with some searching around you can find the most recent version. I was able to find somewhat more recent maps here. The data has to be in the UCSC genome browser somewhere. Most likely you should find your 7000 cM estimate source and figure out which map that estimate comes from if you like that source.

These data structures are called "genetic maps" or "linkage maps". Each chromosome has positions that are defined by cM, and you could use that for your purpose I believe by just taking the largest cM value marker for each chromosome.

(Note that the two copies of a chromosome do not have independent genetic maps- after all, the map is defined by recombination between the two homologs. e.g. for chromosome 1 there is usually just one map, and therefore one maximum cM value- the map is an average across the human chromosomes sampled.)

Edit
The question seems to be related to a genealogical heuristic for identifying relatedness in cM values. I'm still not 100% sure how they measure this exactly.

The source shares expected values for relatedness here: https://secureservercdn.net/184.168.47.225/35b.ded.myftpupload.com/wp-content/uploads/2018/12/Relationship_Chart_FINAL_August_2017.jpg


Population dynamics ODE with Allee Effects

First, Allee effects (also positive density dependence) can be modelled in several different ways, and the equation you give is one example. The terms weak and strong Allee effects are in my experience used in a couple of different ways. Most often, strong density dependence is used to denote Allee effects where the per capita population growth rate can become negative, which means that there is a critical point in population size, below which the population will tend towards extinction. Weak Allee effects are then used to describe cases where the population growth rate is negatively affected by low population sizes, but where the per capita population growth rate cannot go below zero (so populations will grow at low population sizes). Remember that in the classic logistic model, per capita population growth rate is maximized when population size is low (limit towards N=0), while it is maximized between N=0 and N=K in models with an Allee effects (in the model includes a concept of carrying capacity).

Using this definition of weak vs strong,  your model has a strong Allee effect, since per capita population growth rate will go below zero at the threshold A (see below). However, sometimes strong/weak is used to denote some sense of relative influence of the Allee effect on population dynamics, for instance if per capita population growth rate at low population sizes is decreased a lot or a little compared to the logistic model, even if both cases would correspond to a weak Allee effect in the first sense.

For comparison, here are two examples of how an Allee effect can be modelled, that shows how the per capita growth rate is affected with an weak Allee effect (see e.g. Boukal & Berec 2002 and Ferreira et al 2012) or a strong Allee effect (your model):

$$\frac{dN(t)}{dt} = \frac{r}{K}N^2\left(1-\frac{N}{K} \right) \tag{weak}\label{}$$

$$\frac{dN(t)}{dt} = rN\left(1-\frac{N}{K} \right)\left(\frac{N}{A}-1\right) \tag{strong}\label{}$$

If per capita population growth rate (dN/dtN) is plotted against population size for these two models, as well as for the standard logistic model, this is what you get:

In these examples, r=0.7, K=100 and A=20. As you can see, there is a big difference between the weak and strong case. The population growth rate (dN/dt) at different N is shown below:

As you can see, if populations using the strong Allee effect are started below A (in this case 20) the populations will decline towards extinction (since dN/dt is negative below A).

The multi-species extension including species interactions that you propose looks ok to me, for that particular formulation of the Allee effect.

Also, for a flexible way to study the Allee effect, you might be interested in this formulation (see Boukal & Berec 2002), which can produce both a strong and a weak behaviour:

$$\frac{dN(t)}{dt} = rN\left(1-\frac{N}{K} \right)\left(\frac{N}{K}-\frac{A}{K} \right)\tag{flex}\label{}$$

This function will produce a weak Allee effect if $A \leq 0$ (very weak if A is far below 0) and a strong effect is $A>0$. The weak model I give above is a special case of this formulation with $A = 0$. Per capita growth of this model is given below, for two values of A (with r = 0.5 for the logistic model and r = 0.38 for the flex models)

As a sidenote, I've also seen cases where negative density dependence at low population sizes is described as an Allee effect (so that Allee effect can be used to denote both positive and negative density dependence at low population sizes), but this is not very common. For a particular species, negative density dependence at low population sizes (in excess of what is found in the standard logistic model) could e.g. be found in situation where predators have a switching behaviour, so that they stop eating the prey when it becomes rare.


Characters do not make the genus, but the genus gives the characters?

It has been a long time since, I've read The Origin of Species, but it sounds like the intent of the phrase is to suggest that the presence of similar characteristics in two species do not imply that they are related, but that related species would be expected to share characteristics. I.e. that similar characteristics do not imply relatedness, but relatedness implies similar characteristics. Genus -> Characteristics, rather than Characteristics -> Genus. These two possibilities are logically distinct.

The assumption that Genus -> Characteristics segues into the key concept of his theory of evolution, that related species (a genus) arise from the descent with modification of an shared ancestral population. Remember that Darwin wrote long before we understand the role of DNA as the carrier of genetic information. He knew nothing about the physical substance or the mechanism of transmission that passed characteristics to offspring, but through his observations built a strong case that such a substance exists and that gradual changes in this substance occur over time in a population. He later posits that natural selection leads to the accumulation subsets of descendants with modifications that are advantageous in their environment. Thus the species within a genus could arise, their similarities the result of their shared ancestry, their differences that result of descent with modification and selection.


Nomenclature of substrates for DNA synthesis

Summary
The systematic chemical names of many important biological molecules are too long to write routinely in full, and in any case were preceded historically by abbreviated forms which generally stressed the distinguishing features of importance to those studying their metabolism. Thus, as the poster points out, a molecule such as dATP (image below) has a base-(deoxy)sugar-phosphate(s) structure, and can be termed a deoxynucleotide. Adding triphosphate provides the additional information that there is more than one phosphate. A base-sugar(deoxyribose) combination is, as the poster states, a deoxynucleoside, but by extending this name to deoxyribonucleoside triphosphate, one indicates the addition of phosphates, so that one is, by definition, describing a deoxynucleotide. The reference to ribonucleoside indicates that the sugar is ribose, a specification lacking from the other definition. However, in practice these two terms are used to describe the same entity, one which might a little more completely describe as 2′-deoxyribonucleoside triphosphate (to indicate the position of the reductive change). This answer attempts to explain with precision the aspects of the nomenclature that are likely to be important to the biochemist or molecular biologist.
Disclaimer
The original question might be considered not to represent a biological problem, and one might argue for closing it on that account. However because of the very nature of trivial nomenclature, it is difficult for those without experience of the usage in a field to find the answer. In answering it I have tried to broaden the scope to include the aspects of structure that I feel are most likely to be to biological students.
Answer
It is convenient to start with ribonucleoside triphosphates (rather a deoxy- ribonucleoside triphosphates), and I have chosen a specific example in the molecule that is generally known as ATP:

Alternative names for this ribonucleoside triphosphate, in decreasing order of complexity, include:

[[(2R,3S,4R,5R)-5-(6-aminopurin-9-yl)-3,4-dihydroxyoxolan-2-yl]methoxy-hydroxyphosphoryl] phosphono hydrogen phosphate
9-β-D-ribofuranosyl adenine 5′-triphosphate
adenosine 5′-triphosphate
adenosine triphosphate
ATP

Of interest to us are the three components of the molecule: a purine base (adenine), a sugar (ribose), and three linked phosphates. This is not reflected in the chemical nomenclature (1), so let us focus on the, albeit rarely used, biochemical nomenclature (2).

The ‘9’ specifies the position of the adenine ring that is linked to the sugar. This is not of particular interest in the context of the question.  (The numbering of the ring is, however, relevant to describing differences between or modifications  of the purine and pyrimidine bases1.)
The D-ribofuranosyl is a form of ribose (see below). The ‘D’ indicates that it is D-ribose enantiomer rather than the alternative, L-ribose. However, as all natural sugars are ‘D’ this is generally omitted (although discussions of why all natural sugars are ‘D’ abound2).
Ribofuranosyl indicates that the ribose is in the five-membered hemiacetal ring form (rather than the straight chain or the six-membered pyranose ring), but this is always the case in nucleosides, and so is not of particular interest.
The 5′ specifies the position of the sugar ring to which the phosphates are attached, the prime (′) indicating that the numbering is for the sugar ring (not that of the base). This is important, as it is relevant to the linkage in the (asymmetric) phosphodiester bond made to the 3′-OH:

The image above is for DNA, but before addressing the nomenclature there, we would point out:

The common α, β, γ designation of the three bond phospho-ester bonds. This is very relevant to the formation of polynucleotides (DNA and RNA) from their substrates, and in general to the utilization of the free energy the hydrolysis of these bonds for other processes3.

Finally we come to a structure of interest to the poster, dATP:

In the designation, 2′-deoxyadenosine 5′-triphosphate, the 2′-deoxy indicates that it is the 2 position in the ribose ring (′) that has had the oxygen removed (deoxy), i.e. OH is reduced to H. Although common knowledge, it is important that the student new to the subject understands this, as if it were the 3′ position that was reduced, it could not form the phosphodiester bonds of DNA. And it is relevant in many other contexts. For example the chain-termination method of DNA sequencing uses 2′,3′-dideoxy nucleotides to inhibit such bonds forming4, the single difference between ribose and deoxyribose allows us to understand the profound affect on the susceptibility of RNA to alkaline hydrolysis in nature5, and certain RNA molecules are hydroxy-methylated at this position.

Related information in SE Biology answers
1 Topical example related to base modification
2 Speculation on the origin of biological homochirality — not SE Biology
3 Why does ATP sometimes produce ADP and sometimes AMP?
4 Sanger sequencing by chain termination
5 Difference in stability of DNA and RNA


Why is hunting big animals more dangerous for the species?

I can see two different sides to this question.

On one side,

From Darwin's Theory of Evolution, the more adapted you are, the better chance at reproducing you will have, thus passing on your genes.

  "Survival of the fittest" is a phrase that originated from Darwinian
  evolutionary theory as a way of describing the mechanism of natural
  selection. The biological concept of fitness is defined as
  reproductive success.

In this case, you hunt the fittest, strongest animals that can procreate and protect their descendants, leaving the weakest alive. The weakest may not be able to continue the lineage because of their weakest gene pool and the species existence could be at stake.

On the other side,

A reputated Oxford Zoologist, Richard Dawkins wrote:

  We are survival machines – robot vehicles blindly programmed to
  preserve the selfish molecules known as genes

In this particular example, being strong, fit and healthy could be interpreted as being unfit for evolution, since it attracts predators (humans) to kill, as would not be the case for medium sized less meaty healthy individuals. The true adaptation that could make the specie survive in this case is via the weakest members that are not worth the effort to be hunted but still can survive other threats.

There is several more viewpoints that could be described knowing more details about exactly which animals, their environnement, the other predators and the exact contribution of the "healthy strongest" specimens you described as being hunted.

Nevertheless, hunting animals can always endanger the specie depending on the frequency of the hunt, frequency of the animal reproduction and several other factors, so can many other human behaviors.

Source: The selfish gene - Richard Dawkins (Book)


What determines the number of chromosomes an organism carries?

Practically, there is an obvious barrier to changes in chromosome number: haploid cells produced by diploids must contain exactly one copy of each chromosome (or chromosome section, or locus). Otherwise over- or under- expression of genes can lead to dosage problems. Across all of diploids some large groups show strong conservation of number of chromosomes but others seem fairly free to change the number.

An example of conservation are the Drosophilids (fruit flies) where for approximately 100 million years they have maintained five or six chromosomes (search for Muller elements). Incidentally, with a huge amount of intra-chromosomal shuffling of genes "Drosophila 12 Genomes Consortium", 2007, Nature.

An extreme example of changes in chromosome number can be seen between similar species of Muntjac deer . Where in a relatively short time period (of the order of a million years or less (?) - my guess), the number of chromosomes has reduced from 46 to six (Wurster, D. H., Benirschke, K., Jun. 1970). Someone may correct me but I think amongst vertebrates, mammals show particularly fast evolution of chromosome number relative to, say, birds (though more birds also have micro-chromosomes...).

The above changes (or lack of change in Drosophilids) appear to be independent of genome size - so that was a long way round to saying "It's not genome size".

It could be repetitive DNA. The centrosomes (where mitotic spindles attach) of mammals are full of repetitive DNA and for this reason have been hard to sequence accurately (Graphodatsky, A. S., Trifonov, V. A., Stanyon, R., 2011. ). These repeats evolve (in sequence and copy number) and may promote more or fewer spindle attachments. Drosophilids (in general) have fewer repeats but I don't know if this is a diploid-wide pattern [Research anyone?].


What would be required to evolve an animal (non-human) brain to obtain human-level cognition?

Answering the question what is needed for a human brain to evolve starting from a cephalopod brain is hard. However, I can expand on what is thought to have been the driving forces behind the evolution of the humanoid brain (Hawks, 2013):

The species of the famous Lucy fossil, Australopithecus afarensis (~3-4 mln yrs ago), had skulls with internal volumes of between 400 and 550 milliliters, which is comparable to chimpanzees and gorillas. Australopithecine brains started to show subtle changes in structure and shape as compared with apes. however. For instance, the neocortex was expanding, which is an indication that the evolutionary pressure on higher functions of the brain was important.

Homo habilis, the first of our genus Homo, who appeared 1.9 million years ago, saw a modest hop in brain size, including an expansion of a language-connected part of the frontal lobe called Broca's area. The first fossil skulls of Homo erectus, 1.8 million years ago, had brains averaging a bit larger than 600 ml. This shows that language development is a likely factor that has driven evolution of the human brain.

By 500,000 years ago, the humanoid brain reached a volume of about 1,000 ml. Early Homo sapiens had brains within the range of people today, averaging 1,200 ml or more. It is thought that cultural and linguistic complexity, dietary needs and technological prowess took a significant leap forward at this stage, and that our brains grew to accommodate the changes. The shape changes we see accentuate the regions related to depth of planning, communication, problem solving and other more advanced cognitive functions.

Interestingly, in the past 10,000 years of human existence the brain actually shrank. Limited nutrition in agricultural populations may have been an important driver of this trend. Industrial societies in the past 100 years, however, have seen brain size rebound as nutrition increased and disease declined (Hawks, 2013).

Indeed, one of the driving components behind the expansion of the human brain is increased availability of fatty fish to sustain the large amounts of fat needed in a brain - survival of the fattest (Cunnane, 2006).

Although the past does not predict future evolution, a greater integration with technology may lead to further expansion of the human brain (Hawks, 2013).

References
- Cunnane, Med Sci (Paris) (2006); 22(6-7):659-63
- Hawks, Sci Am (2013)


Why do we use cRNA instead of initial extracted RNA in the microarray technique?

After clarification via the comments of the OPs question:

1) The procedure you describe is not for standard RNA microarray experiments, it for olgionucleotide microarray. This type of chip is special because it has multiple probes for each gene to allow detection of special features (i.e. mutations, alternative splicing, ...).

2) The reason for the generation of cDNA with subsequent reverse transcription and biotinylation is not explicitly stated in the source of the OP, but there are some possible advantages:

Amplification of material: cDNA can easily be amplified, which would make it easier to analyse samples whit low RNA yield, genes with low expression levels or to analyse the same sample on multiple chips.
Sensivity: oligonucleotide arrays may use very short (10-25 bases) probes, for which fluorescence readout may not be sensitive enough. Biotinylation of a given RNA base (by the use of pre-biotinylated NTPs during reverse transcription) can give multiple 'marks' on each fragment, which can be read with out streptavidin coupled signals. Additionally this would allow the signal strength to change in respond to certain SNPs/mutations.


Cancer history on environment-cancer relationship

Actually, "soot wart" was identified by Percival Pott in 1775. It is the first reported occupational cancer (it is a squamous cell carcinoma of the skin of the scrotum). It was shown in 1922 that an active ingredient of coal soot was a carcinogen. I'm not sure of an expansive, technical text on environmental cancers, but you may want to check out
"The Emperor of All Maladies: A Biography of Cancer" which covers the origins of man's understanding of cancer starting with the ancient Greeks, progressing to mention Percival Pott, and then moving on to modern day science and medicine. This book won the Pulitzer in nonfiction a few years ago and is well worth your time.


Did humans evolve the ability to swim? Or is it just luck that we are able to swim?

The Jane Goodall website says: "You’ll rarely see a chimp paddling about in the water as they don’t like to swim. Their low body fat ratio causes them to sink and their top heavy body composition makes it difficult for them to keep their heads above water.  However, some chimpanzees do enjoy a good splash around in shallow water."
Some monkeys have been taught to swim, see this video: https://www.youtube.com/watch?v=q2vekGuV8xA
So, the answer is, it's just luck that humans are quite good swimmers compared to other monkeys, because strong bipedal running and legs also gives humans good stability in water. After us the best swimmer is the proboscis monkey. Many other monkeys do play in water and swim: https://www.youtube.com/watch?v=sn-M1kCvzLg
There are many studies that theorize that modern humans have evolved beside seas and rivers.
Here's a massive infographin on the subject: https://visual.ly/community/Infographics/science/possible-aquatic-adaptations-human
Humans crossed the open ocean at least 50,000 years ago, i.e. to colonize Australia, the oldest evidence of fishing is currently from East Timor, 42,000 year old fishing hooks: https://www.livescience.com/17186-oldest-fish-hooks-early-humans.html#:~:text=Their%20discovery%20uncovered%20fishing%20hooks,%2C%22%20O'Connor%20said.


What is the developmental basis of the placental sac?

We used to spend a few days studying the placenta in our embryology course. The short answer is, both.

Organ level embryogenesis:

The placenta connects the fetus to the uterine wall, and is the organ by means of which the nutritive, respiratory, and excretory functions of the fetus are carried on. It is composed of both fetal and maternal portions. The placenta can be traced right from the moment when the blastocyst is implanted into the uterine wall, though it takes a good portion of 12 weeks to develop.

  After this adhesion, the invasion process starts, during which the cytotrophoblast cells from the trophoblast layer migrate deeper into the decidual layer. The formed vacuoles of the embryo become confluent to the uterus with the formation of the lacunar space 13 days after fertilization. The lacunar space will develop into the intervillous space for blood circulation a few weeks later. The placental progenitor stem cell is the cytotrophoblast cell. These cells are responsible for the cellular growth of the placenta, and they have the ability to proliferate and differentiate throughout gestation. The proliferating cytotrophoblast cells provide, after differentiation, the villous syncytiotrophoblasts as the outer cellular layer of the placenta.

I took the above paragraph from here (http://www.medscape.com/viewarticle/780615_2).You can read more about it here (https://embryology.med.unsw.edu.au/embryology/index.php?title=Placenta_Development.)

But for a serious scholarly study, you might be better off using textbooks.

Genetic basis of placental development:

As for the second part of your question, that is the genetic basis of development for a placenta, allow me to lift a paragraph from a book. You must remember that the embryo as it were, is not a distinct entity genetically, in that it contains half of the genes of the mother, and half of the genes from the father. And this is where biology becomes more complex, beautiful and truly mind boggling. It involves intricate interactions between evolution, organogenesis and developmental biology.

  These results [in mice] led to an extraordinary conclusion. Paternal genes, inherited from the father, are responsible for making the placenta – maternal genes, inherited from the mother, are responsible for making the greater part of the embryo, especially its head and brain…

  David Haig had begun to reinterpret the mammalian placenta, not as a maternal organ designed to give sustenance to the foetus, but more as a foetal organ designed to parasitise the maternal blood supply and brook no opposition in the process. He noted that the placenta literally bores its way into the mother’s vessels, forcing them to dilate, and then proceeds to produce hormones which raise the mother’s blood pressure and blood sugar. The mother responds by raising her insulin levels to combat this invasion, yet, if for some reason the foetal hormone is missing, the mother does not need to raise her insulin levels and a normal pregnancy ensues.

  In other words, although mother and foetus have a common purpose, they argue fiercely about the details of how much of the mother’s resources the foetus may have - exactly as they will later during weaning. But the foetus is built partly with maternal genes, so it would not be surprising  if these genes found themselves with, as it were, a conflict of interest. The father’s genes in the foetus have no such worries. They do not have the mother’s interest at heart, except insofar as she provides a home for them.

  The father’s genes do not trust the mother’s genes to make a sufficiently invasive placenta; so they do the job themselves…. Modern evolutionary theorists, led by David Haig, now think of the placenta as more like a parasitic takeover of the mother’s body by paternal genes in the foetus. The placenta tries, against maternal resistance, to control her blood-sugar levels and blood pressure to the benefit of the foetus.

Taken from: Matt Ridley, Genome: The Autobiography of a Species in 23 Chapters, Fourth Estate, 2000

For a more scientific explanation, I'd suggest reading the following papers.

Wang, Xu, et al. "Paternally expressed genes predominate in the placenta." Proceedings of the National Academy of Sciences 110.26 (2013): 10705-10710.

Hemberger, Myriam, and James C. Cross. "Genes governing placental development." Trends in Endocrinology & Metabolism 12.4 (2001): 162-168.


This is a question of convention really.

When people discuss the cell cycle, they usually refer to diploid cells (for diploid animals). So in your context, M stands for mitotic phase and does not directly apply to meiosis.

In meiosis, you could say that the cell also undergo a M-phase (actually two in a row, see footnote) but then the cell cycle becomes irrelevant as you get 4 haploid cells (gametes) that cannot duplicate by themselves anymore, effectively breaking the cycle.

Footnote

The M-phase in the cell cycle is a simplification of the process of cell division as this phase can be further sub-divided into a Prophase, Metaphase, Anaphase, Telophase (PMAT for the purists) followed by cytokinesis. In meiosis, you have a slightly different PMAT process during meiosis I (i.e. 1 cell -> 2 cells) followed by another PMAT (2 cells -> 4 cells). You can find additional information here.


Are you sure that your TBE is at the right dilution? And that you're using TBE to make the gel and also as the buffer for running?  That sort of wavy line looks like what you might get if you'd made the gel with water instead of buffer, or run it with water instead of buffer.  You could also try using TAE to make/run the gel as a sanity check.


Identify this smooth-cocoon worm from Southern India

This is definitely the larvae of one of a many number of case-bearing moth species. As noted in comments and elsewhere, these case-bearing moths show up fairly frequently on Bio.SE (e.g., see here, here, here, here and here for some examples).

Most of these moths are members of one of two families: Coleophoridae (the case bearing moths) or Tineidae (the fungus moths).

Some of these species even build cases that they carry around with them.

Your specific example is possibly Tinea pellionella (case-bearing clothes moth).

[

T. pellionella has a cosmopolitan distribution and occurs nearly worldwide (Cheema 1956). As the Wikipedia article summarizes, the larva feeds mainly on fibrous keratin (e.g., hair and feathers) as well as carpets, furs, upholstery, and woolen fabrics. The larvae remain inside a case it constructs from debris such as hairs and fibers (e.g., from clothing, upholstery, carpets, etc.).


This question is broad.

There are plenty of uses of mathematical modelling in biology.

Wikipedia

You may want to read the wikipedia article: Mathematical and Theoretical Biology.

Books

There are tons of books on theoretical biology. I am personally working in the field of population genetics, a field where much of the theory has been expressed mathematically. Here are book recommendations for this particular field.

On Biology.SE

We have a tag for mathematical-models (you used it in your post). You may want to see what kind of posts are tagged for mathematical-models.

To repeat @fileunderwater's comment, What physics knowledge can be applied to biology of organisms and ecosystems and When are population dynamics models useful? are examples of posts you may want to read.

What prevents predator overpopulation? will give you an example of an easy and classical mathematical model to describe population dynamics of predators and preys.

Personal historical/philosophical note: At some point physicists have started to describe the laws of nature with mathematical expressions and at that time many physicists didn't quite like the idea that physics could be described by math. Biology has gone through the same phase but much later. Early mathematical biologists developed the modern science of statistics (Francis Galton, Karl Pearson, Ronald Fisher). Biologists used existing mathematical tools such as diffusion processes (Kimura). Note that part of the work in the field of diffusion equations have been done by physicist (Einstein solved the 2D equations for diffusion processes). Note also that the dynamic of diffusion processes called brownian motion have been named after a biologist. Today, biology produces massive amount of data that require good computational skills to treat. The time when biologists had only to know how to recognize species is over, now there are few biologists left that aren't able to code in at least one programming language.


Why do zoologists classify sponges as animals rather than plants?

Organisms are classified, not by their behavior, but by their phylogeny (evolutionary relationships). Sponges have unique and complex molecules in their intracellular matrix that developed in a common ancestor of sponges, and are shared with sponges and all other animals. These molecules include collagen, proteoglycans, integrin, and adhesive glycoproteins. These molecules are made by the cells, exist outside the cells, and fill the space between them.


How to give a biological interpretation to this phase portrait?

I don't think you missed anything important!

You could investigate the cyclic behaviour around the equilibrium. For example, looking at the variable aphid population size can start above its equilibrium point, then overshoot it and overshoot it again to finally reach the equilibrium point. If you zoom close to the equilibrium point, you might see long cyclic behaviour before ever reaching the equilibrium.

You sure could do all kind of further analyses such as a stability analysis or searching for cyclical equilibrium but it is easy to see with this simple model that nothing very complicated will arise. You could also investigate for what parameter values this classic pattern breaks up if it does.

Another option is to make the model more complex by introducing a carrying capacity (and then investigate under what aphid growth rate the behaviour becomes chaotic), or population structure, or whatever.

You might learn much from it but you might still want to have a look at the post What prevents predator overpopulation?.

I highly recommend the book A Biologist's Guide to Mathematical Modeling in Ecology and Evolution by Otto and Troy. It will show the typical kind of analyses that can be done for this kind of systems.


Interpreting SNP-in-gene associations from GWAS studies

In short, yes.

If a gwas study links a SNP to a particular phenotype then yes, it is an effect of a single copy. Bear in mind, however, that a SNP is not a knockout or even a knockdown. It can be, but it is not always the case.  SNPs can produce a change in the protein sequence or in the regulation of the production of that protein. Both types of variation can result in a phenotypical change.

In any case, SNP information is always about a single allele, I imagine that you can find cases where a cell is homozygous for a particular SNP but is is not necessarily, or even often as far as I know, the case.


In the literature, it's most common to see hyphenated compound adjectives, like "phage-mediated," "phage-dependent," or "phage-encoded" where "bacterial" or "viral" might be analogous. For example, "Phage‐mediated selection and the evolution and maintenance of restriction‐modification."
Sometimes "phage" seems to be used as a standalone adjective, like in "Phage antibodies: filamentous phage displaying antibody variable domains." Although I'm not sure that it would be correct to use "bacterial antibodies" or "viral antibodies" in this case, so maybe that one is an anomaly.
I would suggest following one of these trends, unless you want to do a lot of explaining to reviewers.


Why does Hunger lead to the aggressive behavior?

Brain's main energy source is glucose. It uses about 20% of total glucose [1]. Brain hypoglycemia causes depressive-like behaviors in mice through adrenergic pathways [2].
When it comes to humans, here is a study that claims low glucose leads to increased aggression in married couples (see this too):

Self-control requires energy, part of which is provided by glucose. For 21 days, glucose levels were measured in 107 married couples. To measure aggressive impulses, each evening participants stuck between 0 and 51 pins into a voodoo doll that represented their spouse, depending how angry they were with their spouse. ... As expected, the lower the level of glucose in the blood, the greater number of pins participants stuck into the voodoo doll, and the higher intensity and longer duration of noise participants set for their spouse [3].

However, the conclusion is disputed:

Bushman et al.'s study does not demonstrate that fluctuations in blood glucose affect individuals' self-control abilities. As an important consequence, there is no reason to assume that giving couples a sugary “boost to their self-control energy” (p. 3) will reduce intimate partner violence. Because the glucose model of self-control lacks empirical foundation, it does not qualify as a framework for scientifically based intervention strategies [4].

What is sure, is that hypoglycemia activates sympathetic nervous system:

... the neurogenic symptoms of hypoglycemia are largely the result of sympathetic neural, rather than adrenomedullary, activation [5].
Hypoglycemia increases plasma levels of both epinephrine and norepinephrine. These catechols are released primarily from the adrenal medulla. However, it is well documented that hypoglycemic increases muscle sympathetic nerve activity, and that both alpha and beta adrenergic activity increase [6].

And this leads to behavioral changes (at least in animals):

Noradrenaline is involved in many different functions, which all are known to affect behaviour profoundly. ... Part of these effects may arise in indirect ways that are by no means specific to aggressive behaviour, however, they are functionally relevant to it. Other effects may affect brain mechanisms specifically involved in aggression. Hormonal catecholamines (adrenaline and noradrenaline) appear to be involved in metabolic preparations for the prospective fight; the sympathetic system ensures appropriate cardiovascular reaction, while the CNS noradrenergic system prepares the animal for the prospective fight. ... It appears that neurons bearing postsynaptic alpha2-adrenoceptors are responsible for the start and maintenance of aggression, while a situation-dependent fine-tuning is realised through neurons equipped with beta-adrenoceptors [7].

References:

Wikipedia contributors, "Human brain," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Human_brain&oldid=615456836 (accessed July 6, 2014).
Park MJ, Yoo SW, Choe BS, Dantzer R, Freund GG. Acute hypoglycemia causes depressive-like behaviors in mice. Metab. Clin. Exp. 2012 Feb;61(2):229-36. doi: 10.1016/j.metabol.2011.06.013. PubMed PMID: 21820138.
Bushman BJ, Dewall CN, Pond RS, Hanus MD. Low glucose relates to greater aggression in married couples. Proc. Natl. Acad. Sci. U.S.A. 2014 Apr 29;111(17):6254-7. doi: 10.1073/pnas.1400619111. PubMed PMID: 24733932.
Lange F and Kurzban R (2014) Sugar levels relate to aggression in couples without supporting the glucose model of self-control. Front. Psychol. 5:572. doi: 10.3389/fpsyg.2014.00572
DeRosa MA, Cryer PE. Hypoglycemia and the sympathoadrenal system: neurogenic symptoms are largely the result of sympathetic neural, rather than adrenomedullary, activation. Am. J. Physiol. Endocrinol. Metab. 2004 Jul;287(1):E32-41. doi: 10.1152/ajpendo.00539.2003. PubMed PMID: 14970007.
Hoffman RP. Sympathetic mechanisms of hypoglycemic counterregulation. Curr Diabetes Rev. 2007 Aug;3(3):185-93. PubMed PMID: 18220670.
Haller J, Makara GB, Kruk MR. Catecholaminergic involvement in the control of aggression: hormones, the peripheral sympathetic, and central noradrenergic systems. Neurosci Biobehav Rev. 1998;22(1):85-97. PubMed PMID: 9491941.


Why do some animals try to imitate other animals?

Mimicry, in biology, phenomenon characterized by the superficial resemblance of two or more organisms that are not closely related taxonomically. This resemblance confers an advantage—such as protection from predation—upon one or both organisms through some form of “information flow” that passes between the organisms and the animate agent of selection.

This link describes different types of animal mimicry

  The two step mechanism of mimicry evolution states that,

  1) Mutations at genes of major effect first allow a phenotypic leap
  achieving an approximate resemblance to a particular model.

  2) Once these mutations have increased in the population, resemblance can be enhanced through the gradual selection of epistatic
  modifiers.

Considering the case of butterflies, the working of two step mechanism evolved through different types of natural selection process. Experiments show that birds associate certain patterns in the butterfly wings to identify the specie and generalize those features, but a small deviation from the exact pattern is neglected. The increased resemblance is advantageous to species having imperfect mimics. So the species which displays/perform imperfect mimics can some how fall under the list of rejection and manages to survive, thereby passing genes to next generation.

  "Largesse of the Genome", an idea put forward by J.R.G.Turner states that, it is believed that the modification of a trait can be achieved by so many different genes that some of them will inevitably happen to be linked.Amoung the many possible combinations of the loci, selection could simply sieve out the ones that involve linked genes.

  Encyclopedia of Insects by Vincent H. Resh, Ring T. Cardé

Although the exact mechanisms of mimicry is still a questionable area, experiments are giving hopes regarding the two step mechanism and more over natural selection is the predominant factor which makes a mimicry successful.

This link describes insect mimicry and two step mechanism in detail.

  References

  A Dictionary of Birds

  Encyclopedia of Evolution

  Rapidly Evolving Genes and Genetic Systems


What limits the speed of human perception?

Flicker Fusion Threshold:

The wikipedia definition:

  It is defined as the frequency at which an intermittent light stimulus appears to be completely steady to the average human observer.

Background

In 1824, Peter Mark Roget (who also wrote the famous Thesaurus) first presented the concept of "persistence of vision" to the Royal Society of London, as the ability of the retina to retain an image of an object for $\frac{1}{20}$ to $\frac{1}{5}$ second after its removal from the field of vision.

A second principle - the $\phi\ phenomenon$ or stroboscopic effect is closely related to flicker fusion. It was first studied by Max Wertheimer and Hugo Munsterberg between 1912-16. Wertheimer and Munsterberg found that subjects can perceptually bridge the temporal gap between two consecutive displays, so that a series of static images appear as continuous movement. The discovery of flicker fusion became the perceptual basis for moving pictures, television, and all media based on stroboscopic presentation of stimuli.

The minimal frequency at which flickering stimuli appear continuous is called the critical flicker frequency.

Perceptual factors affecting the critical flicker fusion threshold

This critical flicker fusion threshold depends on the stimulus’

Luminance (the Ferry-Porter law),
Size (the Granit-Harper law),
Color,
Retinal eccentricity,
Background Luminance, and other factors.

Biology Behind it:

  Physiological evidence in humans and monkeys shows that flicker rates
  above the perceptual critical flicker frequency threshold can
  nevertheless generate cortical and subcortical visual responses.  Thus
  the temporal integration underlying flicker fusion does not occur at
  the level of the retina,  but must take place later in the visual
  hierarchy. Single-unit recordings in the primary visual cortex of
  primates suggests that,  for two brief-duration targets presented in
  close succession, the after-discharge to the first  target interferes
  with the onset-response to the second target (Macknik, 2006) (see
  Figure 5). The onset-response to the second flash is absent for
  inter-stimuli intervals of 30 msec or shorter (equivalent to 17 Hz
  periodic). If the flashes are separated by more than 30 ms, the
  after-discharge to the first flash and the onset-response to the
  second flash begin to recover (i.e. equivalent to <17 Hz flicker).
  These intervals roughly coincide with the critical flicker fusion
  threshold in humans for 100% contrast stimuli in the fovea .

  This suggests that perceptual flicker fusion may be due to the lack of
  robust transient responses to the flickering stimulus.

http://images.scholarpedia.org/w/images/thumb/8/8b/Flicker_fusion_fig5.png/360px-Flicker_fusion_fig5.png

Source:

Bartley (1939). Some effects of intermittent photic stimulation. Journal of Experimental Psychology 25, 462-480.
Bloch, A. M. (1885). Experience sur la vision. Comptes Rendus de Seances de la Societe de Biologie, Paris 37, 493-495.
Brücke, E. (1864). Über den Nutzeffect intermittierender Netzhautreizungen. Sitzungsber k Akad Wissensch Math-naturw Cl, Wien 49, 128-153.
Di Lollo, V., and Bischof, W. F. (1995). Inverse-intensity effect in duration of visible persistence. Psychol Bull 118, 223-237.
Ferry, E. (1892). Persistence of vision. Amer J Sci 44, 192-207.
Fukuda, T. (1979). Relation between flicker fusion threshold and retinal positions. Percept Mot Skills 49, 3-17.
Flicker Fusion

What is the Different speeds of Visual Perception?

First-order motion

Experiment: A moving sinusoidal grating with bright peaks and dark troughs is seen through a window.

Result: Even when its velocity is so high that 30 of its bright peaks pass each location per second (30 Hz), observers still perceive its direction of
motion.

Depth from binocular disparity

Experiment: Two identical gratings, one in each eye, are viewed through identical windows.

Result: One is spatially shifted relative to the other, introducing a binocular disparity that is perceived as depth.
Even when they move at a 30 Hz rate, the depth is still perceived.
If the input to depth mechanisms were blurred at a >30 ms timescale, detecting the depth would be impossible at this rate.

Edges and texture boundaries

Experiment: Against a gray background, a field of white dots is adjacent to a field of black dots.

Result: Both fields are set in rapid alternation between white and black, but out of phase – when
one is white, the other is black. The conspicuous boundary between them is perceived even at fast
rates of 30 Hz, whereas at faster rates the black and white are averaged by the brain into the same color as the background.

http://ak.picdn.net/shutterstock/videos/3139525/preview/stock-footage-retro-geometric-dot-background-in-black-gray-and-white.jpg

Binding of color and orientation sharing a spatial location

Experiment & Result: If a red, right-tilted patch is alternated with a green, left tilted patch,
it is easy to distinguish from the complementary pairing of red left alternating with green right, even at
fast 20 Hz rates.

Binding of form and color across space

Alternating color-shape pairings can only be reported at rates below ~3 Hz.

source: http://www.psych.usyd.edu.au/staff/colinc/HTML/dynamics.htm

Binding of global form with color

Two specially constructed dot patterns that form distinct shapes alternate, with all the dots of one red and all the
dots of the other green.

At alternation rates faster than several a second it is very difficult to determine the shape color pairing even though the shapes and colors themselves
are easily identified.

Direction change and acceleration perception

A moving stimulus alternates between two speeds (acceleration) or two directions. When the alternation occurs
faster than several per second, these changes are unperceivable.
Its limit is 8-10 Hz.

Word perception

Certain pairs of words (such as ‘jump’ and ‘pink’), when alternated in the same location, cannot be distinguished
from another matched pair at rapid rates as one perceives only the sum, which is the same for both pairs.
They can be distinguished only at rates slower than several items per second.

Source: http://www.psych.usyd.edu.au/staff/alexh/research/words/

Source:

Holcombe AO (2009) Seeing slow and seeing fast: two limits on perception. Trends Cogn Sci 13:216 –221.
http://www.psych.usyd.edu.au/staff/colinc/HTML/dynamics.htm


Can you identify this insect (orange back, 6 legs)?

It is a harlequin ladybird larvae.

This is one of the most variable species in the world, with an unusually broad range of color forms. It is native to eastern Asia, but has been artificially introduced to North America and Europe to control aphids.

I figure that Wiki is saying "it has some of the highest color variability of any wild plant or animal".

wiki: harlequin ladybird


Solvent Accessibility, the 20% cut-off method

Its 1.  Below cutoff, buried, above cutoff accessible.

Paper 1: "A cutoff of 20% was used to define the two states, buried or exposed. With this definition, the dataset was, roughly, evenly split between the two states."

Only two states are possible: solvent accessible and buried.

Paper 2: "A given residue is defined as exposed (e) if its RSA is larger than the cutoff
value, and otherwise it is defined as buried (b)."

Abstract for Paper 3: a cutoff of 20% for two-state definition of solvent accessibility.

If it were def #2 it would be a three state definition.

Paper 4: "On average, 15% of residues in small proteins and 32% in larger ones may be classed as “buried residues”, having less than 5% of their surface accessible to the solvent..."

This paper, by the dean of structural analysis Cyrus Chothia, uses a 5% cutoff, not 20%...

The abstract goes on to say... "The accessibilities of most other residues are evenly distributed in the range 5 to 50%."

This passage hints that SA doesn't even go up to 80%.  Just considering that you often won't get more than say 60% with this calculation.  I'm just guessing; but the thought being that unless you are at a terminus of the protein, which is often disordered and doesn't show up in a crystal structure, you will have two adjoining amino acids for each residue - just the solvent accesible area taken up by the contact with neighbors could easily be 20% of total.


In DNA replication, are there phosphodiester bonds in the primer ? between the RNA nucleotides before being replaced

A primer is by definition a short single strand of nucleic acid (i.e. a series of nucleotides linked together by phosphodiester bonds). See also this wikipedia article.


Do any plants exhibit hormonal changes similar to puberty?

In flowering plants (the angiosperms) there are several developmental transitions in the life of the plant. I won't list the plants, because the list includes pretty much all of them (although the magnitude in the change of developmental pace differs widely between taxa and environments).

First there is seed germination, which is controlled hormonally. Absence of germination is usually imposed by abscisic acid, whilst germination is caused at the appropriate time by gibberellic acid and ethylene (among other things; Holdsworth, Bentsink & Soppe, 2008).

Next, in many herbaceous species there is a transition between a spreading growth stage (e.g. rosette growth) and the flowering stage. The 'growth spurt' here is the differentiation and elongation of the flowering stem, and then subsequently the sudden flowering of buds. The transition is also controlled hormonally, by a variety of hormones including auxin (Zhao, 2010), gibberellic acid, ethylene (Schaller, 2012), and the long anticipated, recently confirmed florigen (Choi, 2012). Ethylene and abscisic acid then play important roles in the next developmental transition when seeds and fruits are produced and dehisced.

Small RNAs are also now being revealed to play a large role in controlling the timing of developmental, but they are upstream of the hormonal changes. In particular some key miRNAs are involved in auxin-based regulation of branching, and in embryogenesis (Nodine & Bartel, 2010), and RNA silencing is involved in the switch from rosette growth to flowering growth (reviewed in Poethig, 2009 and Baurle & Dean 2006).

 Bäurle I, Dean C. 2006. The Timing of Developmental Transitions in Plants. Cell 125: 655–664.
 Choi CQ. 2012. A Blossoming Field of Research: How Florigen Is Transported to Create Flowers. PLoS Biol 10: e1001311.
 Holdsworth MJ, Bentsink L, Soppe WJJ. 2008. Molecular networks regulating Arabidopsis seed maturation, after-ripening, dormancy and germination. New Phytologist 179: 33–54.
 Nodine MD, Bartel DP. 2010. MicroRNAs Prevent Precocious Gene Expression and Enable Pattern Formation During Plant Embryogenesis. Genes Dev 24: 2678–2692.
 Poethig RS. 2009. Small RNAs and developmental timing in plants. Curr Opin Genet Dev 19: 374–378.
 Schaller GE. 2012. Ethylene and the regulation of plant development. BMC Biology 10: 9.
 Zhao Y. 2010. Auxin Biosynthesis and Its Role in Plant Development.


Even if we restrict ourselves to Morus rubra, the native species, versus Morus alba, the species introduced from China, and ignore possible hybrids, I think you may have to wait for the trees to be larger for an ID.  I found a relevant paper (Nepal, M.P., M.H. Mayfield, C.J. Ferguson. 2012. "Identification of eastern North American Morus (Moraceae): Taxonomic status of M. murrayana." Phytoneuron 2012-26: 1–6.) which contains the following paragraph:

  Salient features for correct identification of M. alba and M. rubra

  Morus rubra can be easily distinguished from M. alba using
  morphological characters of the leaf, bud, branch, bark and
  infructescence. Leaf characters present a challenge because of the
  tendency for leaves of juvenile shoots to converge in morphology among
  these species. Nearly all of the unique characteristics of M. rubra
  fail in juvenile leaves. Leaves of M. rubra (5–40 x 3–28 cm) are
  larger overall than those of M. alba (2–20 x 1.5–18 cm). In M. rubra
  leaves, the adaxial (upper) surface is rough and dull green (vs.
  smooth and lustrous) and the abaxial (lower) surface is usually
  densely hairy with erect trichomes evenly distributed (soft to the
  touch); the base is often cordate (heart-shaped); the apex is acute,
  acuminate to subcaudate; marginal teeth are often pointed; and the
  color of the main veins is more or less like the color of the lamina
  on the underside. Leaves of Morus alba are usually deep green and
  lustrous adaxially and have few hairs concentrated along the main
  veins on the abaxial surface; the base is rounded (vs. cordate); the
  apex is obtuse; the marginal teeth are fewer, relatively larger, and
  rounded; and the primary veins (underside) contrast more with the leaf
  surface than in M. rubra. The winter buds of M. rubra have bud scale
  margins with a darker (almost black) apical band, while in M. alba,
  the bud scale margins are uniformly brown. Morus rubra has grayish
  bark with flattened, thin plates that peel outwards in age. Morus alba
  bark has thick and solid ridges that are more of a reddish tan
  coloration. The orientation of branches in a mature M. rubra is
  somewhat planar (flat) and spreading like an umbrella. In M. alba the
  orientation of branches is more erect or spreading, and the plants
  appear more rounded or bushy as a result. The fruit of M. rubra is
  longer and narrowly cylindric, while in M. alba it is typically ovoid
  or ellipsoid.

This might be very useful for mature trees, but note the line "Leaf characters present a challenge because of the tendency for leaves of juvenile shoots to converge in morphology among these species. Nearly all of the unique characteristics of M. rubra fail in juvenile leaves."

There is also a recent, purely genetic analysis of the mulberries freely available at PLOS One but I don't think it's too helpful in this context other than it confirms that hybrids are common.

The Phytoneuron paper and a number of internet sites generally point to M. rubra being densely hairy on the underside of the leaves as one of the more important characters.  Your specimens appear glabrous, but the pictures though excellent may still not show tiny hairs well.  If we trust this character in the young plants then we would lean toward M. alba but as stated above, you may have to wait and see.


Parameters for Fitzhugh-Nagumo model of Action Potential

This is actually not the Fitzhugh-Nagumo model of the a neuron, however it is highly related to it. I believe the the Equation you have there, is capable of oscilations for any positive values of $\epsilon$, $C$, $L$. I generated this graph with the parameter values all set to 1.  Note how it is very similar to a sine wave.

I believe you where trying to write Van der Pol's equation here:
$$C\frac{d^2V}{dt^2} +\epsilon (V^2-1) \frac{dV}{dt}+ \frac{V}{L}$$
Note the subtle difference of multiplying by the first derivative.
Here is again a image with all parameters set to 1

The Fitzhugh-Nagumo equation can be found on wikipedia here and on peer reviewed  scholarpedia here. For reference it is a two state model described by the equation:

$$ \frac{dV}{dt}=V-V^3/3-W+I$$
$$ \tau \frac{dW}{dt}= V + a -bW$$

A common value for the parameters are $a=.7$,$b=.8$,$\tau=12.5$ $I$ can be anything really, I used $I=.5$ to generate the graph below. Also note that the model wont spike if I below a certain value. The Fitzhugh Equation is is slightly more general, but does simplify to the Van der pol under the assumption $a=b=0$. Here is the graph of it with the constants I described.


Why do men have a greater chance of suffering from hair loss?

As per my comment above, some types of hair loss is androgenic, and therefore related to testosterone levels. This is why eunuchs can be resistant to some forms of hair loss.


During acid reflux and vomiting, is the burning sensation from pepsin or acid?

It is the acid that causes the burn

Medicines like proton pump inhibitors (e.g. Prilosec), or H2 receptor antagonists (like Zantac) that reduce acid secretion reduce the burning sensation.  Medicines that neutralize the acid like calcium carbonate (e.g. Tums) also reduce the burn.  These medicines do nothing to the secretion of enzymes.

ADDENDUM. @anongoodnurse wants references.  Maybe in exchange she will remove that pesky down vote.

Cimetidine won the team that developed it the Nobel prize - the first rationally (as opposed to empirically) designed drug.  It was designed to very specifically reduce stomach acid.

https://www.acs.org/content/acs/en/education/whatischemistry/landmarks/cimetidinetagamet.html

  Smith Kline & French's multidisciplinary research team first looked at
  the physiological cause of acid secretion. They confirmed that a
  molecule found in the body called histamine triggers the release of
  acid when it binds to a specific receptor (now called the H2-receptor)
  in the stomach lining. Their aim was to find a molecule that
  successfully competed with histamine in combining with the receptor,
  but then blocked, rather than stimulated, acid release. Such a
  molecule was called a histamine H2-receptor antagonist and represented
  a new class of drugs.

This and the successor class of drugs (proton pump inhibitors) are very specifically designed to decrease acid secretion and do little else.

The fact that billions of dollars worth of these drugs are sold means that persons suffering from reflux pain / stomach ulcer perceive that their pain is reduced by a decrease in acid secretion, and so are willing to pay.

  Tagamet® was greeted with great enthusiasm by doctors and patients
  alike. Ten years after its introduction, it had achieved sales of one
  billion dollars and had become the world's number one prescription
  drug.


By What Mechanism Does Heat Cause Muscle Relaxation?

Read this it was very helpful to me as a Reiki Practitioner who wants to know how the heat generated by my hands on therapy with my patients for Hospice brings such relaxation to them.
http://healthyliving.azcentral.com/effects-temperature-muscular-contraction-11504.html


How do insects such as crickets circulate blood through their antennae?

Insects primarily get oxygen through diffusion of air through their skin.  I doubt the antennae need hemolymph circulation.


System biology and evolution: Book-recommendations

Here there are a couple that I own:

The "classic" from Uri Alon touches many of the topics you mention. It is easy to read and goes relatively deep into the methods. There seems to be a new edition (if you search it in Amazon it will pop up), but it was planned for last year's April and then delayed so no so clear when will be actually published. For the original one: Amazon link

Title: An Introduction to Systems Biology: Design Principles of Biological Circuits
Year: 2006
Author: Uri Alon
Publisher: Chapman & Hall/CRC Mathematical and Computational Biology

The other book is this textbook "Systems biology" by  Edda Klipp and others. I attended a talk by Edda Klipp two years ago and she seems to be doing interesting things. This book is more general, covering, somewhat superficially, many topics. It can be good to get a general idea on the field. Amazon link.

Title: Systems Biology Paperback
Year: 2009
Author: Edda Klipp, Wolfram Liebermeister, Christoph Wierling, Axel Kowald, Hans Lehrach, Ralf Herwig
Publisher: Wiley-Blackwell

There are many others (see Amazon results here). Maybe other members can comment on some of the other titles.


Is the birds' decision to fly away congenital or learned behaviour?

This example proves IMHO that migration is largely nature and not nurture:
In the Netherlands, white storks were bred / reintroduced. A large part (about one third?) of the reintroduced birds do not migrate, but their offspring usually does migrate see. They couldn't have learned it from their parents, that's for sure.


How can the phenotypic effects of a tumor suppressor mutation be silenced?

This is more of a comment

Mutation in tumour suppressor is a recessive trait and there is no active "silencing" of the mutation. If a tumour suppressor is a TF then a mutation in the DNA binding domain can have no effect if there is a complementary mutation in its binding site. This is just a theoretical possibility and I have not heard of any examples as such. I don't think any other mechanisms exist for "silencing" any loss of function mutation.


A subgenomic promoter is a promoter added to a virus for a specific heterologous gene, resulting in the formation of mRNA for that gene alone. Many positive-sense RNA viruses produce these subgenomic mRNAs (sgRNA) as one of the common infection techniques used by these viruses and generally transcribe late viral genes. From doi:10.1128/jvi.74.13.5988-5996.2000
So it seems to be an added promoter that helps express certain genes. Often useful in viral engineering.


General Enhancer Questions (Methylation Patterns, ect.)

This subject is actually both complicated and incompletely understood. For example, there is evidence that some enhancers don't result in loops at all — instead their influence travels along the chromatin to a nearby promoter.

You can think of enhancers as being staging areas where protein complexes that promote transcription are assembled. In some cases enhancers are where the RNA polymerase complex is first bound.

When loops do form, this allows the proteins at an enhancer to interact directly with the transcriptional start site.

I think you will find this 2015 review to be a helpful introduction.1

As for methylation (which maybe would be better as a separate question), it is generally true that methylation acts to reduce transcription factor binding and thus decreases transcription.2

However, that overall trend disguises some more complex dynamics.3

References:
1: Pennacchio, L. A., Bickmore, W., Dean, A., Nobrega, M. A., & Bejerano, G. (2013). Enhancers: five essential questions. Nature Reviews Genetics, 14(4), 288.
2: Lea, A. J., Vockley, C. M., Johnston, R. A., Del Carpio, C. A., Barreiro, L. B., Reddy, T. E., & Tung, J. (2018). Genome-wide quantification of the effects of DNA methylation on human gene regulation. ELife, 7, e37513.
3: Sharifi-Zarchi, A., Gerovska, D., Adachi, K., Totonchi, M., Pezeshk, H., Taft, R. J., ... & Araúzo-Bravo, M. J. (2017). DNA methylation regulates discrimination of enhancers from promoters through a H3K4me1-H3K4me3 seesaw mechanism. BMC genomics, 18(1), 964.


Why are flies not scared when landing on a monitor with changing graphics?

Flies see motion. When the monitor screen changes, the visible spectrum of the pixel is changing and nothing is moving.

  Flies have limited color vision. Each color has its own wave frequency, but flies have only two kinds of color receptor cells. This means they have trouble distinguishing between colors, for instance discerning between yellow and white. Insects cannot see the color red, which is the lowest color frequency humans can see. However, houseflies have the ability to see polarized light, but humans cannot differentiate between polarized and unpolarized light. Polarized light is light in which the waves travel only in one plane. [1]

Monitors have polarized film on them so you could test the color hypothesis by taking an old monitor you are willing to sacrifice and removing the polarized film. Then you could test if the flies jump when the screen changes. See here for removing the polarized film on the monitor, or if you have access, this article on A behavioural study of polarization vision in the fly, Musca domestica may hold the answer without needing to ruining a monitor.


In broad way we call it sperm but the motile sperm is precisely called spermatozoon and plural form of spermatozoon is spermatozoa. A non motile male gamete is sperm but not spermatozoon but there is a term for that too its spermatium.


How does an inhibitory synapse communicate to the cell body of a neuron?

An inhibitory synapse works just like an excitatory one!

When a presynaptic neuron fires it will release a neurotransmitter at its terminal(s). This neurotransmitter can be excitatory or inhibitory, the main excitatory one in the central nervous system being glutamate and the main inhibitory one GABA.*

GABA and Glu are far from being the only neurotransmitters in the brain, they're just a classic example, so we'll stick with them. When the neurotransmitter is released it binds to receptors on the postsynaptic neuron (provided, of course, that the postsynaptic neuron expresses these receptors).

Various GABA and Glu receptors exist, both ionotropic (i.e. channel-receptors that let ions flow through the membrane upon binding of the ligand) and metabotropic (i.e. receptors which activate an intracellular pathway that does not per se start the flow of ions, but that can induce it or prevent it indirectly).
For simplicity we'll stick to ionotropic receptors.

Glu binds to three types of ionotropic receptors: AMPA, NMDA and kainate receptors. These have different kinetics/properties, but the bottom line is that they let cations (positively charged ions, such as Na+ and Ca++) into the cell. When this happens a postsynaptic depolarization happens, which is named EPSP (excitatory post-synaptic potential).
So, if the resting membrane potential was, say, -57mV, it will become, for instance -52mV.
This means that, if the threshold potential for firing an action potential were -43mV the cell, which first needed a 14mV depolarization to fire now will need a 9mV depolarization.
If subsequent EPSP sum they can depolarize the cell sufficiently to reach threshold and let the cell fire.

This image from Wikipedia is quite self-explicatory: in this case 3 synaptic events generated 3 EPSPs that summed, making the cell depolarize enough to reach threshold potential, and generate an action potential, that will then propagate to the cell body.

GABA, on the other hand, binds to the GABA-A receptor, which is a chloride channel. In most cases, upon binding of GABA, GABA-A lets Cl- in the cell, effectively hypopolarizing it and generating an IPSP (inhibitory post-synaptic potential). The situation is the same (but opposite) to Glu, this time, though, the potential becomes more negative.

EPSP and IPSP can and do happen at the same time: as they can vary in frequency and intensity depending on the firing frequency and firing pattern of the presynaptic neuron, a pretty much continuous range of voltages can be achieved in the postsynaptic neuron.

Other controls over this process come from metabotropic receptors that can, for instance [de]phosphorylate (add or remove a phosphate group) ion channels modulating their permeability to ions or from the different kinetics of the different channels (for instance certain channels stay open for longer or open in a delayed manner etc), allowing for fine-tuning of the system.

*I am making a gross generalization here. A neurotransmitter is not excitatory or inhibitory per se, it depends on the context. For instance excitatory GABA synapses do exist.


Mendelian dominant trait involved with Hypodontia

Hypodontia isn't a single gene phenotype, but a poli-genic mechanism involved with epistatic phenomenons and environmental scenarios.

The trasmission isn't clear till now, but when you're talking about a poli-gene phenotype isn't so easy to describe the way in which the trasmission is performed. You could find every info about this disease here, in a meta-review study:


If the fitness of a heterozygote is $(1+s/2)$ and of a homozygote is $(1-s/2)$ then why is the probability for a given state $(1+s/2)^j(1-s/2)^{m-k}$

$$\binom mj (1/2)^j(1/2)^{m-j}= \binom mj (1/2)^m~~ ?$$

As you pointed out earlier, in the general case it need not be true that $p = q = 1/2$ but that is what the form of the probability above implies. So the threshold question is why this particular heterozygous-dominant model implies equilibrium probabilities $p = q = 1/2.$ I think the ideas below begin to address this.

The simplest case is for one locus, two alleles, and there are many good derivations online. I think if you understand the situation for one locus you can generalize to higher numbers. (Hopefully I will supplement this answer, time allowing. I think a shortcut would be to assume $p = q = 1/2$ and use your fitness weights. That gives us $\bar{w}=1$ as a denominator. Now for reasons of symmetry I think you can show that the relative frequencies of $p$ and $q$ are equal and so $p' = p.$ Then you have to show that this equilibrium solution is unique.)

For a single locus the derivations of `heterozygote advantage' I have found,(1)(2), assign fitness weights as follows:

AA = (1 - s),     Aa = 1,       aa = (1 - t )

in which $s,t > 0, s \neq t$ in general, from which they derive as a condition for equilibrium

$$\Delta q = \frac{pq(sp-tq)}{\bar{W}}  = 0$$

so

$$\hat{p} = \frac{t}{s+t} ~~~\text{and}~~~ \hat{q} = \frac{s }{s+t}$$

in which $\hat{p}, \hat{q}$ are equilibrum frequencies for each allele, respectively, and s and t are rates of mutation. Nowhere did I see a model in which they had assigned the same fitness to both homozygous cases (AA, aa) but it's just a special case of the heterozygote advantage model.

fitness (AA) = fitness(aa) = (1 - s/2), fitness(Aa) = (1+ s/2).

So if we subtract s/2 from each fitness score (or normalize with respect to Aa to the same effect), we get:

fitness(AA) = fitness (aa) = (1- s ) and fitness (Aa) = 1 as in the two references above, except that now the two homozygous states have equal fitness.

But then we have $$\Delta q = \frac{pq(sp-sq)}{\bar{W}} =  \frac{pqs(p - q)}{\bar{W}} $$

and the only nontrivial solution is $p = q = 1/2.$

So what I am suggesting is that when you assign the same fitness to both $AA$ and $aa$ you no longer have the general case. As for the value of s being forced, the following seems relevant.

The full expression from (2) for the equilibrium condition is

$$p' = \frac{p^2 W_{AA}+ pq W_{Aa}}{\bar{W}} \hspace{10mm}(1)$$

in which$ W_{AA} = W_{aa} =  1- s$ and $W_{Aa} = 1$ and

$\bar{W} = p^2 W_{AA}+2pqW_{Aa}+q^2W_{aa}$

If the homozygotes are assigned the same fitness and $p = q = 1/2$ , equation (1) above becomes:

$$p' = \frac{\frac{1}{4} + \frac{1}{4}(1-s)}{\frac{1}{2} + \frac{1}{2}(1-s)} $$

The program on page 583 of (1) is helpful. Let h:= heterozygous and m:= homozygous. If $p = q = 1/2$ then as long as fitness(h) and fitness(m) are equal the system is in equilibrium immediately.

If $p\neq 1/2$ then as long as f(h) = f(m) the system reaches equilibrium at $p = 1/2$ asymtotically. If $p = 1/2$ but f(h) $\neq$ f(m) the asymtotic limit has to be calculated.

See also http://evol.bio.lmu.de/_teaching/evogen/Evo8-Summary.pdf


Nice pictures! From the back pattern, size, and antennae shape, I'd say this is very likely a Cicada Killer wasp (Sphecius speciosus), cf., for instance, this picture taken at a similar angle to yours.

There are many good resources online about Cicada Killers, including this page from the MSU Extension Office, and the Wikipedia entry Sphecius speciosus.

It would be interesting to see if you could find the distinctive burrow (photo / video) of your resident wasp!


Are there any place in human body that safe to implant things and have large amount of blood run through?

No, there is no safe place.

Devices in contact with blood are subject to thrombosis and embolism. Even devices designed for bio/hemocompatibility are not 100% safe: they are used because the illnesses and diseases they treat are more dangerous than the side effects. Immune responses and platelet activation that occur in the vicinity of a device could also have effects elsewhere in the body, not just in the vessel you could potentially occlude.

Long term, these effects are reduced only because of healing over the exposed surface. You are proposing something which must be in constant contact with blood, which isn't really possible unless you plan to remove and clean it regularly.

On a side note, for the purposes you describe, there are already devices in development based on mechanical motion to do what you suggest (for example, the motion from walking) that are much safer and more feasible than using blood glucose, which is strictly in the realm of science fiction.

Lanzino, G., Wakhloo, A. K., Fessler, R. D., Hartney, M. L., Guterman, L. R., & Hopkins, L. N. (1999). Efficacy and current limitations of intravascular stents for intracranial internal carotid, vertebral, and basilar artery aneurysms. Journal of neurosurgery, 91(4), 538-546.

Wendel, H. P., & Ziemer, G. (1999). Coating-techniques to improve the hemocompatibility of artificial devices used for extracorporeal circulation. European Journal of Cardio-Thoracic Surgery, 16(3), 342-350.

Werner, C., Maitz, M. F., & Sperling, C. (2007). Current strategies towards hemocompatible coatings. Journal of materials chemistry, 17(32), 3376-3384.


I see various exposure limits for carbon monoxide, but what about one breath?

"In any high level CO environment, your exhaled breath CO level will gradually rise but remain lower than the ambient level because you always absorb some of the CO you inhale as long as the level in air is higher than the level in your blood.  As soon as you stop smoking or move to a lower CO environment, you start exhaling."

So I suspect a lungful of pure CO would indeed make you feel awful, but since that wouldn't be nearly enough to replace all the oxygen bound to your haemoglobin, I imagine it wouldn't be fatal in a healthy individual, especially if you were breathing air free of CO after that one lungful.

Apparently it takes 5 hours to eliminate half of your blood CO also.


Specific examples of signalling pathway using logical 'OR' and 'AND'?

There are thousands of examples, here I list just a few.

1) Macrophage activation. This is a complex case with many proteins acting as AND/OR. The following paper depicts a nice scheme that helps to understand the circuit.

https://bmcsystbiol.biomedcentral.com/articles/10.1186/1752-0509-2-36

2) The Lac operon that follows the logic:

if low_glucose AND lactose:
    express(lac_genes)

if (high_glucose OR low_glucose) AND no_lacotse:
    inhibit(lac_genes)

if high_glucose AND lacotse:
    express_at_low_level(lac_genes)

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

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

3) Phosphorylation and ubiquitination pathways. For example,

  ... proteins primed through phosphorylation by one protein
  kinase are often phosphorylated processively on the N-terminal side of
  the priming phosphate by GSK3 at a series of Ser/Thr spaced by three
  residues, with the cluster of phosphates regulating protein activity
  (e.g., glycogen synthase, β-catenin). If the two sites are
  phosphorylated by different protein kinases, then this can in
  principle provide a logical AND gate in a downstream response.

http://www.sciencedirect.com/science/article/pii/S1097276507007988

4) Neurotransmitter signaling pathways.
Figure 2 of the following paper

http://www.sciencedirect.com/science/article/pii/S0022519306003675

describes the boolean logic underlining the signaling pathway

  Tyrosine hydroxylase activates itself in this model.
  There is an “AND NOT” gate between
  tyrosine hydroxylase and COMT to activate dopamine as
  tyrosine hydroxylase and not COMT activates dopamine...

  ...adenylate cyclase is activated by dopamine
  receptor 1 and not by dopamine receptor 2, which has been
  represented by the “AND NOT” gate between the input nodes.

  ...

  DARPP32, is activated by protein kinase A, and
  not by calcineurin, therefore protein kinase A “AND NOT”
  calcineurin activates DARPP32.

  DARPP32 inhibits protein phosphatase1, which is
  represented by the “NOT” gate from DARPP32 for protein
  phosphatase1.
  ...
  The activation of glutamate receptor, needs the presence of both
  protein kinase A and the ligand, glutamate therefore, a
  “AND” gate between protein kinase A and glutamate, “AND NOT”
  protein phosphatase 1. ...

Here the link to a database of natural and artificial biological logic gates and here the article presenting the database

To conclude, I would like to highlight this work on the engineering of a biological transistor.


Anaerobic respiration does not completely oxidize the glucose, and as a result, pyruvate is not completely broken down, yielding fewer ATP molecules, and there are leftover molecules: lactic acid in animals and ethanol in yeast. This is because anaerobic respiration does not utilize oxygen, which is required for the electron transport chain, where most of the ATP comes from in aerobic respiration. In aerobic respiration, the glucose molecule is completely oxidized, and so (through the Krebs cycle and the electron transport chain, which requires oxygen and which produces the majority of the ATP) is completely broken down into carbon dioxide and water.


Why is pepsin able to operate at low pH?

A good question. As you have accurately described, pepsin is indeed a protein, more specifically, a protease enzyme - a catalyst which assists the break-down of protein at certain amino-acid markers such as tryptophan and phenylalanine. As you are likely aware, proteins are composed from approximately 20 amino-acids, as shown below.

However, the chemical properties of a protein are constituted by its folding - its three-dimensional shape. This answer describes some superficial differences between protein families and the mechanism and function whereby pepsin is capable of functioning at a low pH.

Disregarding any post-translational modifications - the alterations made to a protein following translation from mRNA - proteins are made from a determined sequence of amino-acids, named its primary structure. Different classes of proteins shall have a different sequence and proportion of various amino-acids. For example, collagen fibrils are composed from a greater proportion of the amino-acids glycine-proline-hydroxyproline.

A sample of pepsin extracted from a pig (Porcine pepsin) demonstrated a higher yield of asparagine.

Secondary structure - the inter-molecular bonding between amino-acid side-chains including hydrogen-bonding and disulfide bridge. As you correctly described a protein denaturing, it is these bonds which are broken, thereby altering the protein's shape.

Although there be four principal protein structures - primary, secondary, tertiary and quaternary - the first two are most critical to understanding the ability for pepsin to withstand low pH. Pepsin is originally secreted into the stomach as a proenzyme - an inactive precursor to an enzyme - called pepsinogen. When food is ingested, both pepsinogen and hydrochloric acid are released into the stomach. Returning to our primary structure, pepsinogen possesses 44 additional amino-acids compared with the active enzyme. During acidic conditions, the pepsinogen auto-catalyses its own cleavage from the additional strand, folding into the correct form.

Therefore, other proteins in high acidic conditions lose their unique three-dimensional structure due to the breaking of these inter-molecular bonds. In a sense, denaturing only specifies a transformation into an inactive protein but could be stated for pepsinogen which is 'denatured' into pepsin which attains its activity in this 'denatured' form.

For more information regarding pepsin, I would advise the following Wikipedia page as an initial resource: https://en.wikipedia.org/wiki/Pepsin
For information regarding collagen and porcine-pepsin composition, the following sources respectively may help: https://www.ncbi.nlm.nih.gov/books/NBK21582/ and https://www.ncbi.nlm.nih.gov/pmc/articles/PMC427253/?page=2

I wish you good digestion!


Name of dsRNA (or dsDNA) where all strands are identical

Such a nucleic acid sequence is described as a palindrome or palindromic.

Wikipedia has an entry for palindromic sequence in which it is defined as:

  A palindromic sequence is a nucleic acid sequence on double-stranded DNA or RNA wherein reading 5′ (five-prime) to 3′ (three prime) forward on one strand matches the sequence reading 5′ to 3′ on the complementary strand with which it forms a double helix. This definition of palindrome thus depends on complementary strands being palindromic of each other.

It should be noted that this is a description (rather than a name) that is usually applied to segments of larger nucleic acid molecules or to synthetic constructs. I am not aware of a generic name for short dsRNA (or dsDNA) like the one in the question as they are not, to my knowledge, found in Nature and so there has been no reason to devise a name for them. Thus, there are no names for variants either. If you wish to write an article about such things you would need to invent your own terms, but keep well clear of ‘-mers’ (see use of e.g. tetramer).

The sequence presented in the question does not conform to the Wikipedia definition, above, as it has a central mismatch and is therefore not a perfect double-helix. However, as the use of the term palindrome for nucleic acids is a somewhat cavalier extension of the general use of the English word palindrome (an example of which is “ABLE WAS I ERE I SAW ELBA”), I would regard a further minor modification of the Wikipedia author’s definition as unexceptionable.


Cellular Respiration/Fermentation Problem Leading to Lack of Energy

Short answer
(A) is a possible answer and is indeed cause for fatigue, as pyruvate is needed for the Krebs cycle to run. The krebs cycle is an essential step in the generation of ATP in aerobic organisms. (B) is incorrect because NADH is never transported into the mitochondria in any organism (it is a nonsense answer).

Background
NADH is not transported into mitochondria. Instead, its electrons are transported into mitochondria, and I quote from Berg et al. (2002):

  NADH cannot simply pass into mitochondria for oxidation by the respiratory chain, because the inner mitochondrial membrane is impermeable to NADH and NAD+. The solution is that electrons from NADH, rather than NADH itself, are carried across the mitochondrial membrane. One of several means of introducing electrons from NADH into the electron transport chain is the glycerol 3-phosphate shuttle (Figure 18.37).

  Electrons from NADH can enter the mitochondrial electron transport chain by being used to reduce dihydroxyacetone phosphate to glycerol 3-phosphate. Glycerol 3-phosphate is reoxidized by electron transfer to an FAD prosthetic group in a membrane-bound glycerol 3-phosphate dehydrogenase. Subsequent electron transfer to Q to form QH2 allows these electrons to enter the electron-transport chain.

Hence, (B) is incorrect.

EDIT: Now why would lactate be formed in (A)? Pyruvate builds up in the cell, as it cannot be transported into the mitochondria. Since lactate dehydrogenase has pyruvate as a substrate, the equilibrium of this reaction will be pushed to the right and lactate will be formed:

Source: wikipedia page on lactate dehydrogenase

The lack of glucose oxidation takes away the main power supply of aerobic organisms, causing fatigue. Lactate buildup may also induce fatigue.

Reference
Berg et al. Biochemistry 2002, Freeman, New York


How many water molecules will be produced starting from acetyl-CoA in citric acid cycle

Acetyl-CoA has three carbon-hydrogen and one carbon-carbon bond, and it is electrons 'held' in these bonds that are available for biological oxidation.  Thus we say that acetyl-CoA contributes four reducing equivalents. In the TCA cycle, these are transiently passed to NAD+ (to give NADH) and to FAD (to give FADH2): the cofactors may be considered intermediate electron carriers.

It takes 4 electrons (2 reducing equivalents) to make 2 water molecules from 1 O2 (or 4 electrons to reduce 1 oxygen 'atom' to 1 water molecule), but this takes place in the cytochrome oxidase reaction of the respiratory redox chain (with reduced cytochrome C as electron donor), not in the TCA cycle.

It is important to realize that water contributes no reducing equivalents to cellular respiration, and that hydration reactions are neither oxidation or reductions. For water to contribute reducing equivalents, it would have to be 'split', as it is in photosynthesis.

In addition, oxygen is not consumed or produced in the TCA cycle.

The assertion that water can pass electrons to NAD+ in the TCA cycle is an infamous 'textbook error', notably advocated by Efraim Racker in A New Look at Mechanisms of Bioenergetics, and my opinion on this (for what it is worth) is given in this SE answer.

For the role of water in the TCA cycle and the controversies surrounding it, I would recommend the letters by (i) D.E. Atkinson and (ii) Herreros & Garcia-Sancho on TCA cycle confusion published in TIBS and kindly made available by David.  (These references are not indexed by Pubmed and are apparently not available from the TIBS website)


Exocytosis of mast cell secretory granules

Mast cells contain a number of large, granular structures that are regarded as “secretory lysosomes,” yet they share several features in common with large dense-core vesicles, particularly with respect to the mechanisms of exocytosis. Upon activation, mast cells "degranulate" and exotcytose the contents of granules.

SNARE-dependent mechanism mediates exocytosis of neurotransmitters, hormones, and cytokines. Exocytosis of MCG is also SNARE-dependent. SNARE proteins are a family of evolutionarily conserved proteins that facilitate docking of apposing membranes and facilitate the fusion of membranes to accomplish exocytosis. The characteristic feature is a SNARE motif, a stretch of 60-70 amino acids, arranged in heptad repeat. This feature allows SNARE motifs of the individual SNARE proteins (from opposing membranes)  to zipper together, forming a core complex of a four helix bundle. The major SNARE proteins involved in mast cell degranulation include VAMP-8 (integrated in mast cell membrane), SNAP-23 and syntaxin-4 (both plasma membrane bound). There are other layers of regulation of course. The SNARE accessory proteins synaptotagmin 2 (a calcium sensor), Munc13-1/2, Munc18-2 and complexin-2, exert negative or positive modulatory effects on mast cell granule exocytosis (Woska & Gillespie 2012).

EDIT: I don't know about PKC's involvement, but I can speculate that it's part of the signalling pathway after activation of the Fc receptor and upstream of events that initiate mobilization of intracellular calcium, which would then immediately trigger exocytosis. As for movement, if they're like dense-core vesicles, move along actin filaments using a myosin motor (Va or Vb, for example), and in association with Rab-3. This is speculation though, and I'd suggest looking into the literature for more detailed analyses as you are asking for a broad literature review.


The diagram is not clear. They should write "change of oxygen consumption rate".

The caption of the diagram makes it clearer what they are describing:

" In A, a time course for measurement of oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) is shown under basal conditions, [...] ".

So basically they are measuring oxygen consumption rate under basal conditions and apply some chemicals and depict the change in oxygen consumption rate in a diagram, given in percentage.