It's suspected that some protists (namely choanozoans and picozoans) are proper/direct "virus eaters" due to the size of their "eating apparatus" and scarcity of bacterial remains inside them (unlike viral remains), but the evidence is pretty recent; the (2020) study:

used modern single-cell genomics tools to sequence the total DNA from 1,698 individual protists in the water. Each of the resulting Single Amplified Genomes (SAGs) consists of the genome of a single protist, with or without associated DNA: for example, from symbionts, ingested prey, or viruses or bacteria sticking to its exterior. The technique is very sensitive, but doesn’t directly show the type of relationship between a protist and its associates.
The researchers found a range of protists including alveolates, stramenopiles, chlorophytes, cercozoans, picozoans, and choanozoans. Nineteen percent of SAGs from the Gulf of Maine and 48% of those from the Mediterranean were associated with bacterial DNA, suggesting that these protists had eaten bacteria. More common were viral sequences, found in 51% of SAGs from the Gulf of Maine and 35% of those from the Mediterranean, with a frequency of 1–52 virus types per protist. Most were from viruses known to infect bacteria – presumably representing parasites of the protists’ bacterial prey.
But choanozoans and picozoans, which only occurred in the Gulf of Maine sample, were different. These groups, neither of which have chloroplasts, are poorly known. Choanozoans (3–10 µm; also known as choanoflagellates), are of great evolutionary interest as the closest living relatives of animals and fungi. The tiny (up to 3 µ) picozoans were first discovered twenty years ago and originally known as picobiliphytes. Until now, their food sources were a puzzle, as their feeding apparatus is too small for bacteria – but ample for viruses, most of which are smaller than 150 nm.
Every single one of the choanozoan and picozoan SAGs were associated with viral sequences from bacteriophages and CRESS-DNA viruses, but mostly without any bacterial DNA, while the same sequences were found across a great diversity of species.
“It is very unlikely that these viruses are capable of infecting all the protists in which they were found,” says Dr Julia Brown, a researcher at the Bigelow Laboratory for Ocean Sciences and coauthor on the study.
The authors conclude that choanozoans and picozoans probably routinely eat viruses.

The news release also says that how these "virus eater" protists manage to protect themselves against viral infection isn't yet known/studied.
If this needs saying... protists (unlike bacteria) are eukaryotes. I haven't found any source suggesting that any prokaryotes (bacteria or archaea) manage to sustain themselves on viruses.


What is the mass of a single erythrocyte?

It’s not my kind of biology, and I tend to make mistakes in arithmetic, I’ll have a go…

I found a paper by Leblond and Shoucri published in the Journal of Microscopy (1978) 113, 161-170, entitled Calculation of surface area and volume of human erythrocytes from scanning electron micrographs. You need institutional access to read it, but for the human erythrocyte shown below they calculated:

Volume = 85.5 μm3

They found a range of sizes (65 μm3 in another image) so I shall take an average value of 75 μm3.

75 μm3 =  75 × 10–18 m3

Assuming a density of 1.1 g/cm3 for erythrocytes, i.e. 1.1 × 106 g/m3

Mass of an erythrocyte = 83 × 10–12 g (0.08 ng)

This is the same order of magnitude as that calculated later by the poster.

(Apologies for initially quoting the volume in pm3. No idea how I did that — it’s clearly μm3.)


Why do raw prawns turn red after sitting in vinegar?

The prawn has proteins (meat, muscles).

Beef is red because the muscle proteins in it have a molecule that binds oxygen called myoglobin (whereas our red blood cells have hemoglobin that allows them to carry oxygen better).

In fish you know the meat is white because there is no myoglobin present (in the muscle proteins), but another molecule that still binds oxygen but doesn't look red.

When you add heat or acids (vinegar) to the meat, the proteins get denatured, change their shape and their colour too. You get red shrimps by heating the proteins in them.

Hope this helps


Understanding recombination scoring in family pedigrees

Ns are not non-recombinant at the genomic level. What you know is that they do not show recombination events at the risk allele locus as subjects carrying the marker A1 show signs of the disease and similarly healthy subject do not carry the marker A1. Hence they are called non-recombinant. On top of that 3rd generation subjects (excepted III6) show combinations of alleles reflecting inheritance of one allele from each parent.

What is very important is that A1 is not the allele, it is the marker for the risk allele. This means that A1 is not directly the allele but a region of DNA close to the allele provoking the disease, sufficiently close to be co-inherited most of the time with the disease allele.

For III6 you actually know that a recombination must have happened as this subject obviously carry the risk allele (shows the disease) yet not the marker associated with it, therefore a recombination event happened between the marker and the disease allele.


What is the purpose of Y-shaped adapters in Illumina sequencing?

Normally, when you need two unique adapters, say A & B, on either end of unknown insert sequences, cohesive-end ligation is difficult because the insert sequences are "unknown". So you have to do blunt-end adapter ligation, in a reaction containing Unknown Inserts + adapter A + adapter B. This can result in 3 possible versions of insert-ligated product: A-insert-A, B-insert-B and A-insert-B, among which only A-insert-B is the only desired product.

1) Ligation of A-tailed inserts with Y-adapters gives you 100% A-insert-B.

2) Lets now assign a directionality to the insert - say from base 1 to base 400. Following Y-adapter ligation, you will have 2 kinds of insert-ligated products per insert: A-Insert (1-->400)-B and A-Insert(400-->1)-B, both of which are very useful. Each will create a separate clonal cluster and you will get sequence information starting at both base 1 and base 400 of the insert, since in single-read sequencing, the instrument always sequences from Adapter A. However, to know that both these sequences belong to the same insert, one will need to do paired-end sequencing.


What triggers creative thought in humans?

This is a part answer to your question.

The three-factor anatomical model of human idea generation and creative drive presented in "frontotemporal and dopaminergic control of idea generation and creative drive" (Flaherty, 2005) focus on interactions in and between the temporal lobes, frontal lobes, and the limbic system.

Increase in the quantity of idea generation, at times at the expense of quality is associated with changes in the temporal lobe.  Conversely, frontal lobe deficits may decrease the quantity of ideas generated, largely due to judgements of an idea's worth.  The authors assert that interaction between the two mainly affects verbal and some non-verbal creativity
.
Further,

  Mesolimbic dopamine influences novelty seeking and creative drive. Dopamine agonists and
  antagonists have opposite effects on goal-directed behavior and hallucinations.

The authors emphasise that creative drive is not the same as skill, and that the 3-factor model is an alternative to the left and right brain hemisphere skills based model.


Source of information on Biology.SE

This answer offers an introduction to phylogeny on the case study of dinosaurs and birds. If you are not at ease with the concept of monophyletic group, you should definitely have started with this introduction.

This post is somewhat related.

Origin of your misunderstanding

The question is all about nomenclature (and a little bit of semantics). One can call reptiles whatever (s)he wants. The question is what do we define as being a reptile? And the answer is that there are two possible definitions, a common "bad" definition (Definition 1) and a phylogenetic-based "good" definition (definition 2). I think your confusion comes from the use of the same term to mean two different (but related) things.

Definition 1: reptiles

In general, when people talk about reptiles, they talk about turtles, Rhynchocephalia, Squamata and Crocodilia. In this sense, the term reptile is NOT a monophyletic group. In other words, all species being called reptiles (according to this definition) do not share a common ancestor who has no other descendants that the species being called reptiles.

Definition 2: Reptilia

However, there is a defined monophyletic group called Reptilia. Reptilia is a group that contains all Amniota except the Synapsida (mammals and their extinct close relatives). In other words, Reptilia contains all generally called reptiles (as defined above) and all birds as well as all extinct species that are descendent from this same common ancestor.

Exploring the tree of life by yourself

You will find the tree of life on tolweb.org or on onezoom.org (see The best free and most up to date phylogenetic tree on the internet? for more info).

Using tolweb.org: here are the roots of the tree of the Amniota. And you will probably want to search for the Dinosauria (there) and see how closely related they are to the birds but not so much to the turtles.

Addressing your question directly

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

If by reptiles you mean Reptilia, then whether a given dinosaur has feathers, endothermy, or an exoskeleton (!) doesn't change anything to the fact that this dinosaur is a reptile.

If by reptiles you mean turtles, Rhynchocephalia, Squamata and Crocodilia, then whether a given dinosaur has feathers or not doesn't change anything to the fact that this dinosaur is NOT a reptile!

Known Dinosaurs with feathers?

Given that birds are the only animals that have feathers and that birds are dinosaurs, we don't know of any species that has a feather that is not a dinosaur! However, when we think of dinosaurs, we usually don't think about a pigeon.

Of course, the Archaeopteryx had feathers too. Archaeopteryx is an avian (bird-like) dinosaur.

But even non-avian dinosaurs such as Velociraptor probably had feathers as well. More info about how closely related is Velociraptor to the birds (Aves) there on tolweb.org. You probably remember the so-called Velociraptor from Jurassic Park movie (on the left) but here is what a Velociraptor probably really looked like (on the right).

The "velociraptors" from Jurassic park actually look more like a large Deinonychus without feathers than a Velociraptor (Thank you @Gaurav in the comments). However as Deinonychus is much harder to pronounce and way less sexy than Velociraptor, they chose to use Velociraptor in the movie Jurassic Park and deceived an entire generation about what a Velociraptor is! More information about what the species of Dinosaurs the Jurassic Park movie features in the youtube video (in French): Le Vélociraptor from Max Bird.

You might want to have a look at the post Were there any flying dinosaurs? that is very related.

At least, all these big and extinct things with scales are dinosaurs, right?

Well.... not exactly. There are species that you would probably call dinosaurs that we typically don't consider as dinosaurs. Have a look at the MinuteEarth video called "What makes a dinosaur?" for more information in this regard.

Fun and instructive videos

Les dinosaures ont disparu ? from Max Bird and Jamy (in french)
Le Vélociraptor from Max Bird (in French)
What makes a dinosaur? from MinuteEarth


Since Darwinian times, has there been any striking/notable effects of evolution on humans?

Well, "On the origin of species" was published in 1859. If we assume that for humans a generation is approximately 20 years, that means that there have been between seven and eight generations since 1859. That is nowehere near enough time to observe evolutionary changes.

So, in answer to your question, not very different at all.

EDIT:

I think I need to clarify my answer. When we talk about a species evolving or a species being different today than it was X years ago, we are referring to the species as a whole. Of course evolution is an ongoing process, selective pressures are shaping our gene pool constantly. However, in order to say that humans are different today to those of 1859, we would need to show that the prevalence of particular genotypes has changed. That a specific trait (a gene or a mutation in a gene) has become "fixed", or, at the very least, that it has spread to a significant percentage of the population.

@niallhaslam's answer gives a link to a wired.com article about genetic resistance to HIV. This is not something that has recently evolved in response to HIV but is the result of an ancestral mutation. The article itself states that:

  Using formulas that estimate how long genetic mutations have been
  around, researchers have discovered that the mutation dates to the
  Middle Ages.

Granted, this could be a good example of selection in action. If, after many, many more generations, this mutation has spread to the majority, or a significant percentage, of the population, we could point to it as an example of how humans have changed under the selective pressure of HIV infection. In order for this to happen, HIV will have to become common enough that having a resistance to is beneficial to a very large subset of humanity. I would expect to see such selective pressure in, for example, countries like South Africa where 12% of the population is HIV positive. Such pressure, however, will be negligible in countries with lower infection rates. In the US, for example, a recent study found HIV incidence among persons aged 13 years and older to be 42,200–54,000. Since the US has ~312 million people, 54,000 represents ~0.02% of the population. This will not provide enough of a selective pressure to observe differences in the short term evolutionary scale.

We do not, in fact, "evolve quickly in response to parasites viruses etc". Pathogens may apply selective pressure yes. But this is not a quick process. In any case, we do not evolve in response to them. Mutations occur, randomly usually, and if they confer an advantage they may be selected for. Said advantage may be because they confer resistance to disease but even then, the original mutation was not "in response" to the pathogen, However, such selection happens over many successive generations and will spread relatively slowly (quickly by evolutionary standards perhaps, but still slow for us, and certainly slower than 7 generations) across the population. The same holds true of epigenetic changes. Even if they can (as now seems likely) be transmitted down the generations, any selective advantage they confer will still act at the generational level.

So, while we are, of course, constantly evolving, there are no significant differences between the humans of today and those of Darwin's times. Sure, some genotypes may exist today that did not then and vice versa. These, however, are not representative of the species' genome. They may become so after many generations but, even if they exist, they have not had time to propagate through the gene pool and cannot be taken as evidence that H. sapiens as a species is "different" today.


Is there an ecological scenario where terrestrial insect larvae can show food choices?

The diamondback moth (DBM), Plutella xylostella L. (Lepidoptera: Plutellidae) is one of the most important pests of cruciferous crops in the world.. A strain capable of complete development on sugar pea (Pisum sativum L. var. macrocarpon) has recently appeared. A recent study (Henniges-Janssen, Heckel & Groot (2014), "Preference of Diamondback Moth Larvae for Novel and Original Host Plant after Host Range Expansion"; link) compared the feeding preferences of L4 larvae reared during previous larval instars on cabbage and pea. Pea-reared larvae of this strain preferred peas, while cabbage-reared larvae preferred cabbage. L4 larvae of the original strain preferred cabbage irrespective of their previous diet. I don't think this example has been shown to occur in the field, but the two plants are both fed upon by these caterpillars in the wild.

There is also evidence that larvae of Cydia pomonella (codling moth), a marjo agricultural pest of orchards with a near-global distribution, learn to avoid apple flavoured with saccharine if they have previously encountered saccharine-flavoured noxious plants (Pszczolkowski & Brown, 2005); this probably meets your second criterion for ecological relevance more closely (evidence for learning to avoid odour/flavour cues encountered in a toxic plant, thereby increasing survival) but it's less relevant to a real-world field situation than the first example.

I also found an article on associative learning in insects here that may include some useful examples.


What DNA does a self-fertile plant's seedling have?

Selfing (aka self-fertilizing) differs from cloning. When selfing occurs, the offspring is not an exact copy of the parent. When cloning occurs, the offspring is an exact copy (except for a few mutations) of the parent.

Selfing implies that an individual will produce two gametes (typically a spermatozoid and an ovule but that might be a bit more complicated) and these two gametes are fusing to give the zygote (egg or offspring if you prefer).

As a consequence, when selfing, meiosis is occurring (and therefore segregation and recombination) so that the offspring is not an exact clone of the parent but rather some kind of a rearrangement of the parent genome (with a few mutations of course).


That's a wheel bug (Arilus cristatus), a species of assassin bug named for the wheel-shaped projection on their thorax. They tend to prey on pest insects, but they do "bite" humans with their proboscis. The result is an extremely painful, itchy welt, though non-venomous.

These one's don't attack unprovoked, however, so generally just when trying to handle them. You should handle them with gloves.


The process of wound healing is pretty complicated and is much more than only cell division. The woundhealing process starts almost immediately in the moment of the injury and depending on the injury can take quite a long time. Have a look at the figure below (from the second reference), which shows the phases:

Basically this can roughly be diveded into four phases:

Hemostasis/Coagulation:

vascular constriction (blood vessel contraction)
platelet aggregation, degranulation, and fibrinformation (formation of a thrombus and closure of the wound)

Inflammation:

neutrophil infiltration
monocyte infiltration and differentiation into different kinds of macrophages
lymphocyte infiltration

Proliferation:

re-epithelialization
angiogenesis (formation of new blood vessels)
collagen synthesis (formation of new connective tissue)
formation of the extracellular matrix

Remodeling:

collagen remodeling
vascular maturation and regression

This process takes some time and can be prolonged when a wound is infected.  So I don't think there is much room to speed this up, as you need to go through all these phases. This process is also the result of extensive evolutionary processes; otherwise, such complex cooperation between different cells is not possible. For more details on the process itself, have a look at the references.

References

Factors affecting wound healing.
Cellular aspects of wound healing.


I was able to find a reference to the book Good Parrotkeeping by Robin Deutsch (©2009) from a forum post which purports to list several species' call loudness level (sorted by dB):

Nanday conure, 155 dB
Moluccan cockatoo, 135 dB
Mealy amazon, 124 dB
Quaker parrot, 113 dB
Mustached parakeet, 111 dB
Macaw, 105 dB
Mitred conure, 100 dB

I don't have a copy of the book so was not able to check the author's sources. However, I can answer a more general question about how birds are able to make loud noises in general.

Birds have a syrinx instead of a larynx as in mammals. This is situated at the bottom of the trachea, instead of at the top. Given this, birds can take advantage of acoustic resonance, which can allow for some extremely loud calls.

In a 21 Oct 2019 article in the New York Times titled "The Loudest Bird in the World Has a Song Like a Pile Driver" (paywall), the South American white bellbird is said to be the loudest bird in the world at 125 dB. (With the screaming piha now in second place). The study, "Extremely loud mating songs at close range in white bellbirds" was conducted by Dr. Jeffrey Podos and Dr. Mario Cohn-Haft in 2018. Unfortunately, it does not seem to cover the biological mechanics that produce such loud calls, but rather focuses on the evolutionary and sexual pressures that have led to such outliers in avian acoustics.

Edit:

Note that decibels are a measure of acoustic sound pressure, and vary greatly depending on the distance from the source they are measured. In order to be scientifically sound, the loudness of something should be measured from a fixed distance under controlled conditions. Note that the table of examples of sound pressure levels contains a "distance" column, which is extremely important for comparison purposes between sounds. I have no idea whether the parrot measurements were conducted using the same criteria as the white bellbird study (very likely not). Therefore, the higher dB values listed there may be due to measurements with much smaller distances.


What is this insect that I found under my bed

It is a Madagascar hissing  cockroach. They are native to Africa, particularly Madagascar. In the U.S. these roaches only invade homes when accidentally brought in via imported furniture or food, although some people do keep them as pets.

https://en.m.wikipedia.org/wiki/Madagascar_hissing_cockroach


Why would a mother reject her offspring if it has been "interfered" with by humans?

Several ungulates and other species such as seals and primates are known to initially use odour to discriminate their offspring. Most relevant work to study this has been done in sheep; sheep are ideal for studying attachment because there are ethical and logistic difficulties that limit laboratory and research use of most other species known to develop selective mother-young social relationships. In addition domestic sheep are common worldwide, easily bred and handled, and well-understood in terms of behavior and natural history, providing a solid base for more intricate study (more information here).

According to this paper ewes are attracted to amniotic fluid for a few hours after birth, which stimulates nuzzling, sniffling and licking behaviour; after a relatively short time she becomes familiar with the lamb's unique odour. Thereafter, lambs without this odour are almost always rejected. After some time the ewes learn to use visual and auditory cues to identify their lambs and smell becomes less important. The Wikipedia article on the subject gives some information about the neurobiology of the process.

From a selective advantage point of view, I would speculate that this would evolve to reduce the risk of being exploited by 'free-loader' genotypes that engage in behaviour similar to brood parasitism in birds (i.e. leaving their offspring to be cared for by other ewes).

This can work both ways; in addition to the risk of disrupting the smell of a lamb by excessive handling, shepherds have recognised for centuries that lambs which are rejected by their own ewe, or whose ewe has an inadequate milk supply, can be fostered by other ewes who have lost lambs using a technique historically called skin-grafting, where a dead lamb is skinned and the skin tied around the foster lamb. The odour is thus transferred to the foster lamb for long enough for the ewe to accept it and become familiar with its visual and auditory identifiers, after which the odour is no longer important. The paper I cited above above describes a study that found that cloth 'stockinettes' could be used in place of a skin to achieve the same outcome.

edit: Interestingly, the responses to this question at skeptics.SE suggest that the popular notion that odour-based attachment results in abandonment following human interference with birds is probably untrue.


I know that you already picked an answer, but I found an alternative answer for you. On average a person consumes 550 litres of oxygen in a day. Now, our body could burn carbohydrates or fats or proteins to produce energy. Each litre of oxygen can produce 5.04 kcals if it burns carbohydrates, produce 4.68 kcals if it burns fats or produce 4.48 kcals if it burns proteins (reference). That being said, if I consider that all 550 litres were used to burn carbohydrates, a total of 550 x 5.04 kcals will be produced which is 2780 kcals.


Flattening the double helix, i.e. making it look like a ladder (like in the usual diagrams of DNA, shown in the first figure below), would not be possible because of bond angles.

Figure 1

Figure 2

The only way for everything to be flattened out completely (as in Figure 1), is for all the bonds to be planar. However, we know that this is not true, as the C1 (carbon 1) is sp3 hybridised, not sp2, which means that the bond from the sugar to the nitrogenous base is not planar. The bond with the phosphates is also not planar. Hence it would be impossible to flatten DNA out like paper.

Moreover, there are relatively strong London dispersion forces between the layers of bases in the 3D structure (helical form). You can see on Figure 2 that the bases lie parallel to each other in each "step" of the helix. This adds to the stability of the molecule.

To answer your second question about whether DNA would be functional if flattened out, the answer would be no. The helical shape of DNA means that there is a minor groove and major groove, which is a property of its 3D shape. This is where proteins bind, which will help the process of replication (duplication) and transcription ("controlling" cells).

Figure 3


Why are there no endoparasitic mammals or reptiles or birds?

Short answer size.

endo/ectoparasites need to be small to go unnoticed, and be hard to eliminate. The smallest mammals and birds are still much larger than a flea, fluke or other endoparasite. That's why larger parasites leave after feeding, if a vampire bat hung on the cow indefinitely the cow would eventually notice and do something, something as simple as rolling over could kill them quite effectively. While an animals infested with fleas can not do much to get rid of the fleas. The few large endoparasites either evolved from much smaller parasites (tapeworms) or exploit some strange insensitivity in the host(cymothoa) This means there is no path to ectoparasite which could lead to endoparasite.

Why there are endoparasites evolved by other means in vertebrates what exactly would they evolve from, there are no birds or mammals that would survive being cut off from outside oxygen or passing through a digestive system. It is like asking why no flying trees have evolved there just is no path to get there or from where they are now, or if there is a path it is so unlikely that it has not occured.


Inflorescence is a flowering shoot that bears more than one flower. There are two types of inflorescence Cymose and Racemose. Of the two types of inflorescence Cymose inflorescence is more primitive and Racemose is derived. (Parkin 1914)

Racemose

In this type of inflorescence the main axis does not end in a flower, but it grows continuously and develops flowers on its lateral sides in acropetal succession (acropetal (adj.) - of leaves or flowers; developing or opening in succession from base to apex ).

Acropetal sucession is observed in raceme, the simplest racemose
inflorescence.

Now Capitulum or Head, it is another type of racemose inflorescence in which

  the main axis or receptacle becomes suppressed, and almost flat, and the flowers (also known as florets) are sessile (without stalk) so that they become crowded together on the flat surface of the receptacle. The florets are arranged in a centripetal manner on the receptacle, i.e., the outer flowers are older and open earlier than the inner ones.

In the following L.S. of sunflower you can see the disc florets developing/opening in centripetal manner.

P.S. I'm not a botanist but a candidate of B.Sc Zoology. I had Botany as my additional subject so I answered it from my knowledge.


After transcription of some UsnRNAs, the RNAs leave nuclei first. After assembly of various proteins and modification on the RNAs in cytosol, the RNAs come back to nuclei. In addition, it has been shown that mature U6snRNP shuttles between nuclear and cytosolic fractions in yeasts, if I remember correctly.

http://openi.nlm.nih.gov/detailedresult.php?img=2582628_gkn658f1&req=4


Does a queen wasp sting also have poison?

Yes, all female wasps are expected to have venom. In the case of social wasps, which I am inferring is what stung you, all female wasps are equally potent as they're morphologically the same. [This opens the question of how could you say this was a queen wasp.] The only difference between a wasp worker and a queen is that a worker is forced to fly around and forage by the queen so it doesn't have the time and energy to invest into laying eggs.

The following paper discusses this: http://dx.doi.org/10.1590/S1519-566X2008000600011

However, not all individuals are the same, both wasps and people, so you may have been stung by a rather weakened wasp/species to which you're not particularly sensitive.

I'd like to recommend the following paper which isn't about wasps, but discusses fundamental venom composition differences between fire ant workers and queens.

Fire Ant Queen Venom is Fire Ants' Secret Weapon
This is the DOI reference: http://dx.doi.org/10.1016/j.toxicon.2018.11.428

(Free Version)
This is the DOI reference: https://doi.org/10.1101/454637

Contrary to wasps, most species of ants present a marked caste specialisation, meaning queens are quite different from workers. However, they still produce (and deliver) venom.

Thanks for your account!


What is the function of the human eye white?

Short answer
The relative large surface area of the white sclera in humans has been linked to an enhanced ability to detect eye gaze.

Background
The white of the eye is caused by the sclera. Human eyes indeed have the highest relative amount of visibly exposed white sclera. The amount of visible sclera provides information about the orientation of the eyeball. Specifically, the iris-to-sclera ratio is an important cue for eye gaze perception (Schulze et al., 2013).

Eye gaze is important. Most mammals generally interpret direct gaze as threatening, or as a sign of dominance. Humans, in contrast, tend to associate mutual gaze with positive interest, love and attraction. A preference for direct gaze seems to be present at a very early age. Infants as young as 2 days old prefer to look at faces that gazed directly at them, than to faces with averted gaze. Yet, humans sometimes find eye contact uncomfortable, for example if a stranger keeps staring at them (Schulze et al., 2013).

The ability to detect gaze has been established in many primate species, other than humans. Gaze detection may have evolved because direct gaze can signal that a predator is attending, making its detection an important tool for survival. Many animal species respond to the presence of staring eyes with displays of fear and submission, indicating that such stimuli act as warning signal. In humans, prolonged eye contact can also be perceived as an aggressive approach signal, as it leads to increases in galvanic skin response (Frischen et al., 2007).

The cooperative eye hypothesis assumes that the large scleral surface in humans developed especially for gaze detection (Tomasello et al., 2007). The authors base this conclusion on the fact that human infants mainly followed gaze, while several species of great apes (including gorillas and bonobos, but not macaques) mainly followed head movements.

However, from my humble opinion, concluding that humans developed a large relative surface of white sclera for communication purposes is kind of far-stretched. For one thing, macaques also have quite a large white scleral surface (Fig. 1.) and macaques share a dedicated neural circuit with humans that involves the superior temporal sulcus (STS). The STS is thought to process biological motion, including gaze. The STS projects to the amygdala, a structure of the limbic system that implicated in the processing of the emotional content of stimuli, including facial expressions and gaze detection. It links this information to emotional responses in the observer. There are also connections between STS and the intraparietal sulcus, an area that is associated with spatial processing and shifts of attention. Via these connections, information about eye-gaze direction could project to spatial attention systems to initiate orienting of attention in the corresponding direction, as in joint attention. Indeed, passive viewing of a face with averted gaze elicits a stronger response in the IPS than viewing a face with direct gaze (Frischen et al., 2007).

Fig. 1. Macaque. Source: Fine Art America

Personally, from these data I think the brain in humans and primates like the macaques adapted to process the information available from the eyes. It can be true, however, that brain circuits and eye structures developed/evolved in parallel to ultimately result in a large white scleral surface and a dedicated neural circuit to process its information.

References
- Frischen et al., Psychol Bull (2007); 133(4): 694–724
- Schulze et al., Front Hum Neurosci (2013); 7: 872
- Tomasello et al., J Human Evol (2007); 52 314-20

Further reading
- Frans de Waal


Short answer
Blue color is not only rare in edible organisms - Blue color is rare in both the animal and plant Kingdoms in general. In animals, blue coloring is generated through structural optic light effects, and not through colored pigments. In the few blue-colored plants, the blue color is generated by blue pigment, namely anthocyanins. The reason for the scarcity of blue pigments remains unknown as far as I know.

Background
The vast majority of animals are incapable of making blue pigments, but the reason appears to be unknown, according to NPR. In fact, not one vertebrate is known to be able to. Even brilliantly blue peacock feathers or a blue eye, for example, don't contain blue pigment. Instead, they all rely on structural colors to appear blue. Structural colors are brought about by the physical properties of delicately arranged micro- and nanostructures.

Blue morpho butterflies are a great example of a brilliant blue color brought about by structural colors. Morphos have a 6-inch wingspan — one side a dull brown and the other a vibrant, reflective blue. The butterflies have tiny transparent structures on the surface of their wings that scatter light in just the right way to make them appear a vibrant blue. But if you grind up the wings, the dust — robbed of its reflective prism structures — would just look gray or brown.

Similarly, the poison dart frog is blue because of the iridiphores in its skin, which contain no pigment but instead feature mirror-like plates that scatter and reflect blue light (source: By Bio).

Morpho and poison dart frog. sources: Wikipedia & LJN Herpetology

Similarly, in the Kingdom of plants less than 10 percent of the 280,000 species of flowering plants produce blue flowers. In fact, there is no true blue pigment in plants and blue is even more rare in foliage than it is in flowers. Blue hues in plants are also generated by floral trickery with the common red anthocyanin pigments. Plants tweak, or modify, the red anthocyanin pigments to make blue flowers, including pH shifts and mixing of pigments, molecules and ions. These complicated alterations, combined with reflected light through the pigments, create the blue hue (source: Mother Nature Network).

But why the blue pigments are so scarce, seems to be unknown as far as I know (MNN, NPR, Science blogs)

Sources
- MNN
- NPR
- Photobiology


Are these claims of "revolutionising" understanding of human vision and hearing valid?

OK, I'll field this one. I'll ignore any of the tell-tale signs of hokum such as writing in ALL CAPS.

Nevertheless, it's a lot of hokum. It's true that he goes into a lot of detail and I'm sure his math looks nice but the fact is that it's not grounded in reality. I would consider myself to be something of an expert (in training) in the field of phototransduction, so I'll focus on claims related to it. However, if he's as sloppy with the rest of the visual process as he is with phototransduction, then his claims are entirely bogus.  I'll just be working from the Synopsis section.

Where to start...How about the first sentence of the "Background" section:

  This work originated in the 1960's with the realization that rhodopsin, as then defined, did not meet the requirements for being a chromophore.  It was particularly deficient in the structural characteristics required of a good chromophore.

FALSE. Rhodopsin is not a chromophore and, to my knowledge no one has ever claimed it to be a chromophore. Rhodopsin is a protein. It is coupled with a chromophore, retinal, a form of vitamin A. OK, so if this is the foundation of his research, he is off to a bad start.

  The basic assumption had been that the residues of a destructive process could be easily returned to their original state and that state was a simple chemical bond involving only two components in a single molecule...It was assumed that one of the residues was the alcohol or aldehyde of Vitamin A. The other residue was assumed to be a protein and was given the name opsin. Valiant, but unsuccessful, efforts were made to define the nature of the molecule and achieve the formation of rhodopsin in the laboratory.

It absolutely is possible to reconstitute rhodopsin with the chromophore in the lab. This has been going on since at least 1983. Also, the crystal structure of rhodopsin, including the chromophore, was resolved in 2000.

  A new class of retinoids was defined by the author at that time, the Rhodonines. This class met the requirements of physical chemistry and photochemistry for a high performance chromophore. However, it was difficult to obtain acceptance of the Rhodonines as a replacement for Rhodopsin within the vision research community.

I have never heard of Rhodonines and web searches only result in his page. Due to his confusion of terminology, I don't know if he is proposing them to be proteins ("replacement for Rhodopsin") or simple chemical molecules ("a high performance chromophore"). If it were the former, one would wonder why Rhodonines were not identified in a comprehensive proteomics assay of the rod outer segment. One would also wonder why rhodopsin is so highly expressed in the outer segment (on the order of 1e8 molecules in mammals and 1e9 molecules in amphibians, more than any other protein in that compartment). If it were the former, one would wonder why there is an entire biochemical cycle dedicated to recycling retinal that takes place just outside the outer segment.

I'll ignore whatever physical state these Rhodonines are supposedly in since they don't exist. I'll also ignore this "Activa" thing. He owns a patent on it, which doesn't bode well for its existence in nature.

  The visual system is a very sophisticated system. It uses many of the most sophisticated methodologies known to man at the start of the 21st Century. Failure to recognize these mechanisms and methodologies leads to an inadequate understanding of the overall process.

I'll agree there, with the exception of the use of the word "methodologies"! This isn't engineering, this is biology.

  The visual system employs a number of time related processes that have not previously been addressed in the literature. To understand these processes, it is necessary to employ "complex algebra" in the differential equations arena. Employing these techniques provides the complete solution to the overall photoexcitation/de-excitation process within the Outer Segment of the photoreceptor

Phototransduction has a rich history of mathematical modeling. And yes, they involve "complex algebra in the differential equations arena." An excellent review of the first few decades of it can be found in the bible: Phototransduction in vertebrate rods and cones: molecular mechanisms of amplification, recovery and light adaptation. Since that publication, there have been two very nice lineages of models: one comprehensive one that focuses on the proteins (1, 2, 3) and one that focuses on spatial accuracy and stochastic interactions and gives more attention to second messengers (1, 2, 3).

  It has also been compounded by the historically poor preparation of the researchers in the field of mathematics.

I challenge him to read one of DiBenedetto's modeling papers and not glow in admiration of his mathematical prowess.

  The goal has been to present an overall view of the visual system in a defendable mathematical context and a global scientific framework. This goal has required the introduction of techniques and mechanisms not normally found in the literature of vision. This has been particularly true in two areas, the definition and detailing of the initial photodetection process and a similar detailing of the mechanisms of neural signal transmission. In both cases, the dominance of chemically based concepts is shown to have impeded progress. The description of the visual system, including the neural system, as an entirely electronic, more precisely electrolytic, based system leads to much greater insight into the operation of the visual system than any chemically based theory can offer.

I had to quote in full here. This is entirely bogus. The "initial photodetection process" (phototransduction) is entirely chemical in nature. All of the main players in the process are known and their interactions are largely well understood. Viewing the system as entirely "electronic" ignores the mountains of evidence of all of the proteins participating in it.

  Probably the most venerable is that of a dichotomy between types of photoreceptors, the rods and cones. The theory demonstrates in excruciating detail that there is only one functional type of photoreceptor cell and that it is associated with one of four types of chromophore. These chromophores are sensitive in the ultraviolet, the short, the medium and the long wavelength portions of the visual spectrum of light.

The problem with this is that if you look at a retina, you can see rods and cones. You can generate knock-out animals that have only one or the other. Those with only rods cannot handle bright visual stimulii, those with only cones cannot see in the dark. More damning is that you have two distinct phototransduction cascades, separated by evolution dating back to the origins of vertebrates. They share only a few proteins in common and otherwise have unique paralogs performing similar duties. You can isolate individual rod cells and, if you're clever and you have the right species, individual cone cells (they're much smaller and harder to harvest in animals like mice or cows). You can measure their electrophysiological characteristics and find that they are extremely different: cone responses are fast while rods can respond to a single photon of light. Their morphologies are completely different: the rod outer segment is filled with lipid bilayer disks, while that of the cone has a series of in-folds.

As for the whole tetrachromat thing, well, again I have to assume that he's referring to opsins when he talks about chromophores. Thanks to genomics, we can be confident that there are only three cone opsin varieties in old world apes (and one rod opsin). The rest of mammals only have two. If you get into other vertebrates, you'll find more...if you get into invertebrates, you'll find ridiculous numbers. There's not much to say here. A fourth cone opsin protein simply does not exist in the human genome.

So, that's just a quick overview. Do not worry about this guy's research. It is unsubstantiated and exists in a vacuum outside of the rest of the vision research world. I do wish that there were a way for him to work with others. I do wish there were a way for him to integrate current knowledge into his work. But the problem is that his work as it stands simply seems to ignore the wealth of data generated on the visual system and instead treats it as some theoretical circuit.


You have a point there, but it probably does not play a big role. First one arm is not such a big branch, and then the carotids contain the main pressure "sensors", so the heart might just beat a bit weaker/slower. Resistance is higher, but demand is less.

Compressions like that can happen all the time, through weight or muscle tension. If it is not both legs at once, this is only a problem for the blocked-off part, after a while.


At which voltage will the conductance decrease due to the narrow pore in a voltage-gated potassium channel?

There is a point where diffusion into the pore can be a limiting factor in the channel's conductance. If the trans-membrane voltage and the recording solution viscosity are high enough, unitary ionic current departs the Ohms law; approaching a plateau. This asymptotic saturation amplitude represents the diffusion limited rate with which ions approach the channel entrance. The bigger the pore entrance, or the higher the ion concentration, or the larger the diffusion coefficient, the higher is the limiting asymptotic current. The pore entrance is measured as the capture radius.

The diffusion limited maximum unitary current (iDL) is directly proportional to the capture radius of the channel ($r_c$):

$$
iDL=2π z e_o r_c D C
$$

z is the valence of the ion, $e_o$ is the elementary charge, C is the bulk concentration of the ion, and D is its diffusion coefficient.

Here you can find a case in which single channel current is not linear with voltage and an example calculation of the capture radius of shaker $K^+$ channel.


Is there any bank of animations for Embryology?

I don't know of any database, but a short search brought up a few candidates. Depending on what you would like to see, they should be a good start:

Human Embryology Animations
Simbryo (Flash based)
UNSW Embryology
Embryological Development of the human
Embryodynamics


Why do we feel tired if we sleep excessively?

Studies have proven somewhat the opposite of what you're asking

For example a study from 2004 - "The impact of extended sleep on daytime alertness, vigilance, and mood" found that,

  Average daily POMS vigor and fatigue scores also improved during the sleep extension period

And thus concluded

  Extended sleep leads to substantial improvements in daytime alertness, reaction time, and mood.

Whilst an older study from '73 -"Performance and Mood Following Variations in the Length and Timing of Sleep" found that,

  Neither sleep duration, nor any other sleep parameter consistently correlated with the performance or mood measures.

The study does go on to state however,

  Therefore, it seems reasonable to assume that the detrimental effects of acute changes in the length and/or timing of sleep were not directly related to any specific changes in the length or electrophysiological patterns of sleep, but to as yet unknown physiological changes resulting from the disruption of an established circadian rhythm of the sleep and wakefulness.

This perhaps suggests that the question which should be asked should not be why does oversleeping makes us feel tired, but why does the disruption of normal sleeping patterns make us feel tired?


How is CO2 and O2 separated in our body during breathing?

It all comes down to concentration gradients. In deoxygenated blood, which is what enters the lungs, the O2 concentration is relatively low and the CO2 concentration is higher than that of ambient air. On the flip side, the air that we breathe in has a higher concentration of O2 than deoxygenated blood. The alveolar membrane is thin enough that the gases can diffuse across this gradient almost instantly. And just like that, you have oxygenation of blood, and removal of CO2.


What determines the direction in which motor proteins go?

While you're entirely correct that the ABABAB sequence is symmetric to a motor protein cruising along, the individual $\alpha$ and $\beta$ monomers themselves are not symmetric along the axis of movement (or any axis at all, as far as I can tell). This produces a polarity that can be seen in the figure below, from the original 1998 paper describing it.

The figure you use above to display the microtubule is slightly misleading in this way; it shows the subunits as blobby spheres. However, the motor proteins are able to distinguish the top of these molecules from the bottom, seeking a unique set of loops and helices to attach to. As it walks, then, the motor protein can only bind to one side (pole) of the subunit and is unable to walk backwards.


No, this is not a carpenter ant...it's possibly a Pavement Ant (Tetramorium
caespitum) - only it's a male & hence winged....for identification...follow these guidelines-

  Pavement ant workers are small, l/8-inch to 3/16-inch
  long, and blackish brown with light-colored legs and two spines at the
  end of the thorax. A distinguishing character, visible with a hand
  lens or microscope, is the series of fine parallel groves on the head
  and thorax


If you draw blood from arteries,it will spout out because the arterial blood flows at some pressure. Moreover, it is too hard to stick a needle because arteries consist of thick blood walls.


How does the body count time in the short term?

Detection of rhythm is a separate function from general musicality, but both can be affected by the same brain damage, or they can be independently affected:

  A range of rhythmic deficits has been described, including the inability to reproduce rhythmic patterns or to discriminate between them, and the inability to perform music rhythmically, or to keep time to music, including dancing in time. These deficits may occur in combination with other musical deficits, such as impaired vocal and instrumental skills ... rhythmic and metric organisation can be differentially impaired in brain damaged patients, supporting the relative independence of functions of the rhythmic system. In terms of cerebral lateralisation, Peretz and Morais [43] suggested that metric organisation may be ascribed to the right hemisphere, whilst smaller rhythmic groupings are encoded by the left hemisphere. ... Neuropsychological studies of groups of patients, however, have generally shown more variable lateralisation effects, particularly in recent research [25,36,46]

--Modelling rhythmic function in a musician post-stroke

So it seems that the detailed neuroanatomy and function of rhythm isn't completely understood, but it is a fairly specific function.  One suggestion is that it's  linked to language ("We conclude, then, that this effect is linked to language dominance and not handedness." -- Rhythm and dominance), but I don't know how widely this is accepted.  Possibly Common neural mechanisms for explicit timing in the sub-second range. offers more insight, but I don't have access to the full article and the abstract isn't very helpful.


What would be the membrane's form if phospholipid tail lengths vary?

Some the scenarios depicted are not energetically favorable and will lead to very unstable membranes if at all.

In the presence of many short-chain lipids, where the difference in chain lengths is very drastic, it will become more favorable for the membrane to reorientate some of the short-chain lipids such that the hydrophobic gaps/pores in your cartoons convert into hydrophilic ones with the head groups forming the pore walls (see fig. below).

If the difference in chain length between the two lipids is not much, the bilayer will adjust its thickness to minimize the hydrophobic mismatch. In such cases, the bilayer will be thinner in some regions. The possibility of interdigitated bilayers is also very much there and will depend on the choice of lipids in question. Interdigitated lipid membranes have been reported before and you can look it up.


What is the word for a group of genes inherited together?

I believe you are referring to operon?

In genetics, an operon is a functioning unit of DNA containing a cluster of genes under the control of a single promoter. The genes are transcribed together into an mRNA strand and either translated together in the cytoplasm, or undergo splicing to create monocistronic mRNAs that are translated separately, i.e. several strands of mRNA that each encode a single gene product.

There is also a term called supergene which is in a way a less strict grouping, suggesting close genetic linkage and possible functional relationship.


Why seeds won't sprout given excess water?

You've stated in your question that oxygen was sufficient for germination, but if there's too much water this probably isn't the case. It's likely given excess water seeds will drown- that is they have not got access to sufficient oxygen to continue germination.


Is there any reason the common housefly continues to return to an area?

I don't think it's a silly question, but it is a common error to anthropomorphise animals.

Insects respond to cues which they have evolved to respond to, and this is how they 'make decisions'. They do not have free will or any more complex decision-making process like common sense. This is evident is lots of insect behaviour: flying repeatedly at a closed window; landing on brightly coloured clothes instead of flowers; and returning to a food source when they are in real danger of being swatted!

When a fly senses the food (often by olfactory receptors), they are 'programmed' to fly towards it in response to some chemical they sense depending on the species and food. They may not have adapted a response to swatting, or perhaps the food cue overrides others. In nature swatting is not so much of a threat to a fly. Some animals may brush them away, but since they are not really doing any harm in feeding from another animal's food, they are mostly ignored.

CO2 traps are used to entice and kill mosquitoes. The mosquitoes are attracted to CO2 (as it is dispelled from the animals from which they blood feed), they will only evolve to avoid the traps if there is another cue which they could eventually associate with a negative effect.

Another thing to remember when thinking about insect behaviour is that their life strategy is very different to ours. Insects are more r-selected than humans, meaning that each individual life has not had so much energy put into it as a more K-selected animal (such as humans), and to compensate for this, many more young are produced. This often results in more risks being taken by individuals since there will still be a viable population even after many deaths.

Chapter 4 of 'The Insects' by Gullan & Cranston gives a good introduction to the sensory responses of insect behaviour. There are other books on the subject, 'Introduction to insect behaviour' by Atkins looks like a good starting point, but I have not read it yet.


The American Veterinary Medical Association (AVMA) has thought about humane methods of euthanasia quite a bit and has an extensive (102 p. PDF) set of guidelines for the euthanasia of animals. The guidelines are not the same for all animals. Some examples:

Companion animals (e.g., dogs and cats): injected barbiturates are recommended

Laboratory animals (e.g., mice and rats): injected barbiturates are acceptable as are inhaled agents (isoflurane, carbon dioxide).

As for humans, you might look into the physician assisted suicide literature. I think that these generally use a sequence of drugs. As far as natural deaths, kidney failure is supposed to not be very painful.


Does our nose detect only if there is change in odor?

Senses in general adapt to continuous stimulation due to various processes. One such process is simply the exhaustion of the reserves of a receptor, or secondary neuron, due to a depletion of neurotransmitters. Entering a room activates a fresh pool of chemical receptors, thereby generating a clear sense of smell. However, this dims due to adaptation. Exiting and re-entering the room after a while revives the neuronal response. More central adaptive responses may also play a role. A comparable effect is seen in the tactile sense. For example, the awareness of wearing a ring or watch fades quickly. Changing its position revives the percept. So yes, sensory systems like olfaction and touch are more responsive to differential stimuli.


What is actually systematics? What is the difference between it & taxonomy?

Systematics studies the diversification and relationships of past and present living forms. Taxonomy is only a part of systematics as defined by Michener et al. in 1970:

  Systematic biology (hereafter called simply systematics) is the field that (a) provides scientific names for organisms, (b) describes them, (c) preserves collections of them, (d) provides classifications for the organisms, keys for their identification, and data on their distributions, (e) investigates their evolutionary histories, and (f) considers their environmental adaptations. This is a field with a long history that in recent years has experienced a notable renaissance, principally with respect to theoretical content. Part of the theoretical material has to do with evolutionary areas (topics e and f above), the rest relates especially to the problem of classification. Taxonomy is that part of Systematics concerned with topics (a) to (d) above.

Source: Michener, Charles D., John O. Corliss, Richard S. Cowan, Peter H. Raven, Curtis W. Sabrosky, Donald S. Squires, and G. W. Wharton (1970). Systematics In Support of Biological Research. Division of Biology and Agriculture, National Research Council. Washington, D.C. 25 pp.

via Wikipedia contributors, "Systematics," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Systematics&oldid=635316421 (accessed November 30, 2014).


They are the final stage of a mosquito larvae, called "pupa".


carbohydrates and lipids as a source of energy? why?

First, it is a matter of the energy that food can provide. Here fat wins clearly (from the Wikipedia article on Food Energy):

Fat: 37 kJ/g
Ethanol (drinking alcohol): 29 kJ/g
Proteins: 17 kJ/g
Carbohydrates: 17 kJ/g
Organic acids: 13 kJ/g
Polyols (sugar alcohols, sweeteners): 10 kJ/g
Fiber: 8 kJ/g

Proteins and Carbohydrates have approximately the same energy content. But the advantage of carbohydrates (and especially glucose) is that is can be taken up by the body and the cells pretty fast, while proteins need to be digested and broken up, before they can metabolized further. Also plants make primarily sugars (or derivated polymers like starch), so carbohydrates are readily available in the food.
Fat and sugars are chosen for nutritional reasons, since they have a higher energy content and are available for it.

Structural components are build by proteins, since the 20 amino acids allow a much greater diversity in the protein chains than it would be possible for fats or carbohydrates. The building blocks are relatively small and simple but they all have the same basic structure (carbogroup, aminogroup and the sidechain) which allows linking via the functional group and the sidechain influencing their behavior (hydrophobic, hydrophilic, charged, etc.).


Does the process of photosynthesis occur in insectivorous plants?

"Carnivorous plants are plants that derive some or most of their nutrients (but not energy) from trapping and consuming animals or protozoans, typically insects and other arthropods. Carnivorous plants have adapted to grow in places with high light where the soil is thin or poor in nutrients, especially nitrogen, such as acidic bogs and rock outcroppings."

Source: https://en.m.wikipedia.org/wiki/Carnivorous_plant


Genes that exist in old Affymetrix platform but not in the newer one

aI used to work at Affymetrix when most of these arrays were designed.  I was not on the design team itself, but I can maybe talk about this a bit more.

RNA Array designs were built to cover anything that might possibly be real transcript in the mix of EST collections, cDNA, in silico gene detections and miscellaneous entries in public databases.  There were a lot of different people trying to find genes as quickly as possible and a good deal of it was not real gene naturally. I'm sure there was a reasonable amount of contamination in the millions of transcripts we took in as well.

The team would find a good number of errors in the sequence database.  There is no way to submit this in a meaningful way to most bioinformatics databases by the way.  Just a note:)

When a new design came out the team would do auditing to see if any of the transcripts had fallen out of favor with the evidence and some of those 'genes' would be pared from the content.

This is useful because DNA hybridization tech is very high throughput for the dollar but it has a background noise and even a probeset with no correspondence in the RNA sample will give numbers that are non-zero.

RNAseq has similar issues from assemblies and sensitivity from limits of reads on the sample BTW.  There's no perfect solution as of yet.

BTW sometimes genes get renamed. I didn't get into your methods to see if this is a case, but something to keep in mind.


The term intergenic is more or less obsolete now. In fact it is ironical to say that a gene, which can give rise to a functional protein or an RNA, is expressed from an intergenic region. However the usage continues for both lncRNAs and miRNAs (other major type of ncRNA in metazoans1 - piRNAs have different classification). lncRNAs are vaguely classified as sense-overlapping (expressed in the same direction as a known gene but not completely overlapping), antisense (expressed from the antisense strand of a known gene) or intergenic; similarly miRNAs are classified as intronic or intergenic.

It is not necessary that the intergenic RNA has to be strictly non-coding, it can be coding as well; a novel protein.

In all these cases the term intergenic means - not overlapping with a known gene. Better nomenclature is necessary as the field of genomics makes more progress.

See this article.

1 Most metazoans.


Balancing selection and positive selection are not mutually exclusive. Neither are balancing selection and negative selection. Sickle cell is a classic example where there is negative selection against the homozygote for the sickling mutation, and positive selection for the heterozygote. The result is that there both alleles are maintained in the population under balancing selection.


What is meant by electron transfer potential?

the electron transfer potential is based on the difference in the affinity of elements/molecules to bind electrons. the affinity of the element derives from it's components as shown in the elements table, just like all other characteristics. for example, oxygen has higher affinity to bind new electron than carbon. the affinity of the molecule derives from the atoms that build it, their electric potential and the connections between those atoms.

this potential between the two elements/molecules (lets say: NADH, O2, iron–sulfur clusters) holds energy that can start a reaction which will never start otherwise.

I have tried to keep it simple. for more reading about oxidation-reduction ( reactions involve the transfer of electrons between chemical species) read TERMODINAMICS AND CHEMICAL KINETICS p.255 as suggested by @Roland.


Is there a detectable amount of bacterial DNA in the blood of infected persons?

Everything depends upon the infection and on the general immune status of the patient.

Generally, the prerequisite for DNA to freely circulate in the blood is the presence of bacteria themselves in the blood (bacteraemia). This means that the infection left its original site (where it is usually kept isolated from the blood flow by the immune system). Depending upon the body reaction to this breakthrough, sepsis and/or SIRS can be the consequences.

Under these conditions (not necessarily as severe as sepsis, but in case of proven bacteriemia), the bacteria cells get attacked by the immuno cells, that leads to their eventual lyzing and releasing their content to the blood.

PCR can be used as a method to prove the existence of bacterial DNA. (Here is a publicly available paper on this topic).


Is there a relationship between Melatonin, Norepinephrine and depression in humans?

This answer addresses your question about a link between norepinephrine and melatonin, but I have nothing to say about depression.

In vertebrates, the link between norepinephrine (NE) and melatonin lies in the regulation of the melatonin biosynthetic pathway.

Arylalkamine N-acetyltransferase (AANAT) is an enzyme in the biosynthetic pathway for melatonin, and controls the diurnal rhythm of melatonin production in the pineal gland. NE is released as a neurotransmitter by neurons innervating the pineal gland, and which themselves are regulated by the circadian pacemaker of the hypothalamus. One of the effects of NE on the pineal gland is to elevate the transcription of the AANAT gene via adrenoreceptors and cAMP levels.

The paper cited below describes this, and other relevant diurnal rhythms in the viscacha, a rodent of the chinchilla family. This animal was chosen because it has an interesting diurnal behaviour pattern with two apparent peaks in melatonin biosynthesis. It's a good starting point for further research into the literature on this topic.

  Calderon,C et al. (2008) Daily rhythms of norepinephrine, β1-adrenoceptor mRNA, serotonin, arylalkylamine N-acetyltransferase mRNA, arylalkylamine N-acetyltransferase and hydroxyindol-O-methyltransferase activities, and melatonin in the pineal gland of viscacha. Biological Rhythm Research 39: 93-107


Is the genetic term "polycistronic" still used in modern biology?

Yes, it's still used.

If you search Pubmed for "polycistronic", it offers you a chart showing the counts of the term by year (top right). Downloading the CSV and making a chart shows that it's never been a very common term, but it's still used. I suspect, but don't have time to check, that if you were to divide the use of the term by the number of published papers by year its use-per-paper would be pretty much a flat line.

Edit, re-reading the question, it may be about "cistronic" as opposed to "polycistronic". "Cistronic" is also still used, but not nearly as often as "polycistronic" -- 13 times in 2018 to "polycistronic's" 81.


Why is the pituitary gland located in the brain?

The evolutionary pressure on the location of the pituitary is likely not the reason why it resides at the basis of the brain. Instead, its (partly) neural origin makes it anatomically (and functionally) part of the brain. Why would it migrate out of the brain when it doesn't have to? What would the evolutionary pressure be on increasing the length of the axons connecting it to the other parts of the brain? It is part of the brain, hence it is located there. It clashes with the principle of parsimony to have the pituitary evolve to a structure located farther from the brain.

The neuroanatomy of the pituitary is schematically as follows (Fig. 1):

Fig. 1. Pituitary gland. Source: Imagekb.

The posterior lobe of the pituitary gland consists largely of extensions of processes (axons) from the hypothalamus and are part of the neurohypophyseal system. There are neural connections to the brain and other centres of the hypothalamus. Hence, the posterior lobe is neural tissue.

The cells constituting the anterior lobe of the pituitary gland are embryologically derived from an outpouching of the roof of the pharynx, known as Rathke’s pouch.


Apologia

This answer was prepared in response to a previous question about Measles virus, but the question was removed for reasons I am not party to but which I can guess. As I spent some time on it I thought I’d post it in reply to this question. It is specific for measles virus, although there are obviously aspects that apply to other viruses, and deals with characterization as well as isolation. I am not a virologist (although I have done some biochemical work on pig herpes virus) so the it was is based solely on my reading of the papers cited and of Field’s Virology. I welcome suggestions for corrections or additions. It may seem to some that the question does not justify an answer of this detail. However it may also be of interest to young contemporary students and researchers who may have difficulty in envisaging the technological limitations of post-war experimental science.

Original Isolation and Characterization

The Edmonston strain of measles virus was isolated in 1954 by Enders and Peebles from the blood of a child with measles, David Edmonston. Before this scientists had found that an agent which was small enough to pass through filters that retained bacteria (i.e. possibly a virus) could cause measles when inoculated into monkeys and could be passaged in eggs containing developing chick embryos — the best method available until then. What Enders and Peebles managed to do was to maintain the virus in cells growing in tissue culture (a far more convenient host experimentally) — initially primary human kidney cells, and then monolayer cultures of chick embryo cells.

They used light microscopy to detect the changes in the cells that demonstrated that they were infected (the original paper contains many photographs of the cytopathogenic effects on infected cells). They could passage the virus by inoculating uninfected cells with infected cells, and they also isolated some virus from the cells by breaking open the cells and using the technique of centrifugation to separate the (larger) virus particles from the soluble cell contents and debris. (Subsequently much improved purification procedures were developed, resulting in preparations suitable for electron microscopy.)

One of the main techniques for characterizing viruses at this time was immunology. Thus, they found that the tissue culture fluid reacted with the antibodies in serum from measles patients by the complement fixation test, showing that it contained measles antigen. Previously they had showed that the cytopathogenicity of their preparations was neutralized by such antibody-containing serum.

Their paper ends with a summary of the evidence that what they isolated was the viral agent responsible for measles, and the further evidence needed for conclusive proof.

Subsequent characterization

The subsequent 60 years saw a steady improvement in analytical method, so that characterization did not rely solely on observation of cell pathology and immunology (the methodological repertoire of which also developed immeasurably). Electron microscopy in the 60s allowed cellular infection to be followed in greater detail and, after improvements in purification, the structure of the virus itself to be observed. The nucleic acid, protein and lipid envelope components could also be analysed with such purified virus.

The emerging techniques included gel electrophoresis of proteins (to determine their size and relative abundance, and to effect small-scale preparations). Larger scale purification of the virus proteins was possible with purified preparations, allowing  amino acid sequencing, especially of the most abundant proteins (e.g. the nucleocapsid protein, N),  and cDNA cloning and sequencing technology led to the sequencing of the whole Edmonston virus genome by Bellini et al. in 1985. This latter resulted in a much greater understanding of the gene expression of the virus, and provided tools such as specific oligonucleotide probes for various genes and antibody reagents to detect specific proteins.

Comment on Poster’s specific questions

The crux of the argument in the question would seem to be:

  “If a researcher filters the particles in a serum…any sample filtered by size will potentially have hundreds of different viruses in it, all the same size range…”

The above addresses this only implicitly. To be explicit:

Using either the serum from patients infected with a specific virus, virus passaged in eggs or viruses grown in cell culture one is massively increasing the proportion of that virus to any contaminants.
It is not easy to grow viruses in cell culture. Therefore when conditions are found for one virus they are unlikely to be optimal for other (low-level) contaminants. Thus the actual passage in culture removes viral contaminants. The purification problem becomes one of separation from cell debris.

Modern Methods of Purifying Measles Virus

Below is a summary flow chart taken from the article Manufacture of Measles Viruses by Langfield et al..

One of the key methods in this proces, Tangential Flow Filtration, is also known as Cross-Flow Filtration and is described in this Wikipedia article.


Watermarks visible during DNA fingerprinting?

The "watermarks" that you're referring to sound exactly like DNA fingerprints: stretches of DNA that are unique to an individual. These unique stretches occur naturally in all individuals, but specific artificial sequences could theoretically be inserted via techniques such as CRISPR.

Once inserted, these artificial sequences could be searched for specifically through PCR, if the sequence is known, or through traditional enzymatic restriction methods, such as described in the first link.

It's worth mentioning that in order to be easily detected, your watermarks would most likely have to be inserted into the germ line of these genetically modified humans. Otherwise, you'd only be able to get the watermark sequences into a small region of tissue. Once in the germ line, the body's own DNA replication mechanism takes over copying those sequences throughout the organism.

Good luck writing!


Difference between null and recessive allele?

To add to Remi b's answer - this question is confusing because 'null' and 'recessive' are terms emerging from two very different levels of analysis. The concept of 'recessive' existed before we knew what genes were, or how they worked. It just describes the patterns of inheritance you see in a gene's effects.

The concept of a 'null' allele however came later, and explicitly describes how an allele works - by destroying gene activity. So 'null' is molecular concept, 'recessive' is an abstract genetic concept. It so happens that null alleles are very often recessive, because usually one working copy of a gene is fine. But the two terms are describing genetics at very different levels.


Some of the plants that respond to mechanical stimuli:

Dionaea muscipula

  'Venus’ Flytrap (Dionaea muscipula) accomplishes one of the more spectacular thigmonastic movements resulting in a swap of the role of predator with animals (Simons, 1992). Indeed, Darwin referred to it as ‘one of the most wonderful in the world’ (Darwin, 1893). The specialized bi-lobed leaves with needle-shaped tines on the leaf margins are generally spread open as invitations to visitors. When an unsuspecting insect crawls along the ventral leaf surfaces and bumps into the three small trigger hairs (Curtis, 1834), intercellular electrical signals are generated (Burdon-Sanderson, 1873; Jacobs, 1954; Jacobson, 1965; Simons, 1981) and are thought to trigger differential enlargement of lobe cells (Fagerberg & Allain, 1991), resulting in trap closure in less than a second. Generally, multiple stimulations of one or more of the trigger hairs are required for a response.1

Drosera rotundifolia

  Distinct touch-induced carnivorous behavior is demonstrated by Drosera rotundifolia, a species examined in detail by Darwin (Darwin, 1893). The mucilage on the ends of the Drosera's tentacles glisten in the sunlight (Fig. 2a,b) and give the plant its common name ‘Sundew’. Over 100 tentacles can cover the surfaces of its modified leaves. This showy appearance attracts insects, which upon alighting on the tentacle surfaces become trapped in the gluey substance. The tactile sensitive tentacles detect the presence and further movements of the insect as it struggles to be released. In response, neighboring tentacles bend towards the ones directly stimulated by the prey's presence.1

Utricularia (Bladderwort)

  The Utricularia trap, attached via a stalk to the rootless plant body (Fig. 3a), is a thin-walled hollow sac with a watertight trapdoor. When the trap is set, the outer walls are concave and the chamber is under negative hydrostatic pressure. Various appendages, some with mucilage-secreting glands, have roles in luring prey to the trap door entrance and others near the bottom of the door are the touch-sensitive triggers. Small creatures, such as water fleas, are examples of those that fall prey to Utricularia traps.1

Mimosa pudica

  Mimosa pudica, known as the sensitive plant, and some of its relatives are other well-known thigmonastic plants. A touch stimulation results in a very rapid folding up of the small leaflets composing the doubly compound leaves. Remarkably, the touch response is not restricted to the stimulated leaflet, but can propagate to all the neighboring leaflets of the leaf (Simons, 1981; Malone, 1994). A stronger stimulus, resulting in wounding, can elicit folding behavior at distantly located leaf petioles (Simons, 1981; Malone, 1994).1

Bryonia dioica

  Elmar Weiler and colleagues have found that an increased level of octadecanoids, in particular 12-oxo-phytodienoic acid (OPDA), correlates with touch-induced Bryonia dioica tendril coiling (Stelmach et al., 1998; Blechert et al., 1999) and that OPDA, and related analogs that cannot be converted to jasmonic acid (JA), are sufficient to cause tendril coiling with physiologically relevant kinetics in the absence of a mechanical stimulus (Weiler et al., 1993, 1994; Blechert et al., 1999).1

Monstera (Vine)

  The Monstera vine has an unusual technique for finding a host tree to climb. It travels by growing along the ground in search of the darkness of a tree's shadow; this movement towards darkness is called skototropism (Strong & Ray, 1975). The vine completes its journey when the vine apex senses arrival at the host tree by the resulting touch encounter. A dramatic change in growth direction then occurs. The Monstera vine begins an upward climb of its host tree (Strong & Ray, 1975), and leaf and stem development changes in anticipation of increased light and productive photosynthesis.1

Ficus costaricensis (Strangler fig)

  The strangler fig (Ficus costaricensis) has a more sinister interaction with host trees (Putz & Holbrook, 1986; Putz & Holbrook, 1989). Roots of the epiphyte form grow downward from its host tree and, in addition to wrapping around the trunk, roots that touch each other fuse together (Fig. 5). As the roots continue to grow and fuse, they eventually encircle and prevent further growth of the host trunk. Further differentiation of the fig's roots result in such constricting pressure that it damages and eventually kills the host in a manner befitting its name. In this way, the strangler remains alone without competition from its former host.1

Catasetum (Flower)

  Male flowers are poised to respond to visitors that contact antennae in the center of the flower by the release of stamen filaments held under tension by petals. The force by which a sticky disc with pollen sacs hits the chosen pollinator can be strong enough to knock a bee from the flower (Simons, 1992). This experience and the burden of the attached large pollen sac can be so traumatic that the bee will carefully evaluate potential future visiting sites and strongly prefer female flowers rather than the explosive male ones (Romero & Nelson, 1986). In this way, male Catasetum flowers may have evolved to compete for exclusive pollination rights of female flowers (Romero & Nelson, 1986).1

Arabidopsis

  When Arabidopsis roots encounter glass barriers, gravitropism appears to be compromised and thigmotropism occurs instead. The touch-stimulated roots neglect their propensity to grow towards gravity vector and instead grow away from the perceived point of mechanical contact. The interaction of touch and gravity may occur at the subcellular level; touch can delay one of the earliest known graviresponses, the falling of starch granules in the root columella cells (Massa & Gilroy, 2003).1

References:

 1) In touch: plant responses to mechanical stimuli [Janet Braam]

 2) Thigmomorphogenesis: a complex plant response to mechano-stimulation [E.Wassim Chehab ; Elizabeth Eich ; Janet Braam]


Atherosclerosis can develop in high pressure systems, such as arteries, and not in low pressure systems, such as veins. It is high blood pressure that can damage the lining of the blood vessel and initiate the process of atherosclerosis.

BUT, atherosclerosis can develop in veins that have been used as grafts instead of arteries, for example, in a coronary artery bypass surgery.

Springer: Atherosclerosis:

  In this regard, we may note that atherosclerotic lesions do not
  develop in the veins in their normal environment of low pressure and
  high flow, but that the lesions do develop when the veins are used as
  arterial bypass grafts where they are subjected to high pressure.
  Similarly, atherosclerotic lesions develop in the pulmonary arteries
  only in pulmonary hypertension.


How do people digest fat after gall bladder removal surgery?

This is not a problem, since the gall bladder "only" stores bile, but the production itself happens in the liver. There are some cases described which can get problems digesting very fatty food, but for most people this is not a problem. Additionally eating low-fat food in the first few weeks after the removal is recommended. See here for some more details.

The picture below shows the location of the gall bladder and also the bile ducts (picture from here)


Genes (here defined as protein coding sequences) are not perfectly aligned the ones after the others in the genome. In fact, in humans (like in most eukaryotes), only a small fraction (of the order of the percent) of the genome directly code for proteins.

Each gene translation unit starts with specific markers. Not even talking about what will be or won't be transcribed, a translation unit starts with the start codon (AUG). Hence, a frameshift mutation will only affect the gene in which (or even, only the exon) in which the mutation happened.

For writing a software that finds coding sequences (and translate them), you will need to learn much more about genetics. You might want to have a look at an intro course on molecular genetics / central dogma / translation, transcription such as a number of the biology classes on Khan Academy for examples.


Why are there splice variants within the same organism? What might contribute to the need for the feature?

The reason is very simply to provide enough variation in a limited sized genome to produce the repertoire of proteins produced by the cells of multicellular organisms. It is also a matter of efficiency and reduced energy consumption.

Consider that on average there are about 100,000 unique protein types being produced in a human cell [1], but the human genome is estimated to contain only 19,042 protein coding genes [2], then the cell needs some way to vary that limited instruction set.

Also remember that differentiated cell types express certain genes but not others, and produce different proteins that other cells do. So that implies that there are more than 100,000 different types of human proteins, and far fewer than 19,042 genes being expressed in any one cell at the same time.

So without splice variants, our genomes would either need to be far larger than the approximately 3 billion base pairs it is already or our repertoire of proteins would be significantly less. We would also have a lot of redundancy, as many common exons would have to be repeated over an over again. That would require a lot more energy for DNA synthesis, and nucleic acid synthesis, etc. The process would become inefficient rather quickly and would likely make complex multicellular animal life untenable.

There is a bit of an error in your question. Splice variants are identified by the mRNAs that are produced, and exons are defined by the sequence that is in the mature mRNA. Introns are, by definition spliced out of the pre-mRNA, meaning that splice variants are not "produced by different combinations of introns and exons." Splice variants will only consist of different combinations of exons. The only time an intron would be found in a mature mRNA is if a splice site is mutated and it is no longer recognized by the spliceosome, so it leaves the intron in incorrectly. This will generally result in a non functional protein.

EDIT

  The collection of components required to carry out the intricate processes involved in generating and maintaining a living, breathing and, sometimes, thinking organism is staggeringly complex. Where do all of the parts come from? Early estimates stated that about 100,000 genes would be required to make up a mammal; however, the actual number is less than one-quarter of that, barely four times the number of genes in budding yeast. It is now clear that the 'missing' information is in large part provided by alternative splicing, the process by which multiple different functional messenger RNAs, and therefore proteins, can be synthesized from a single gene.

-Expansion of the eukaryotic proteome by alternative splicing: Nilsen and Graveley

  Alternative splicing of pre‐messenger ribonucleic acid (pre‐mRNA) allows the generation of different mRNAs from the same gene. Evolution of alternative splicing affecting translated regions of mRNAs permits the synthesis of different proteins from a single gene, significantly increasing the diversity of the protein repertoire.

-Patthy, László(Apr 2008) Alternative Splicing: Evolution. In: eLS. John Wiley & Sons Ltd, Chichester.

Also while I am not one to accept a Nobel Prize at face value, they are usually awarded when the field accepts the explanation of the hypothesis. The 1993 Nobel Prize in Physiology and Medicine was awarded to Richard J. Roberts and Phillip A. Sharp "for their discovery of 'split genes'."


Human somatic cells have 22 pairs of homologous chromosomes?

Answer: *Yes  , human somatic cells have 22 pairs of homologous chromosomes

The human genome consists of 46 (2n*(22+1) ) chromosomes.

Most of our cells are somatic and diploid (2n), they have two homolgous chromosoms (called homologs, one "father" & "mother") these cells multiply by mitosis.

Reproductiv cells or gonosomal cells, (gametes; Sperm and eggcell(ovum)) are the product of meiosis ( a part of gametogenesis ) . These cells are haploid (1n), they only have one set of chromosomes (1n * (22+1)) which is a combination of "fater&mother". When 2 gametes  combine a diploid zygote is formed.

In both cases (Mei- and Mitosis) chromosome (pair (2n)oder single(1n)) number 1 -22 are called autosome , while

Chormosome number 23 is an allosome (sex chromosome), either Y (male) or X (female).

Since the gametes are haploid (1n) they have only 1 single allosome, egg cell always X , and  sperm cell either X or Y.

If the allosome (the 23 chormosome pair) of an human is hemizygot ( X–Y ), he is genetically male. Is the allosome pair X-X
,homozygot the person is genetically female.

Somatic cells can have therefore 22  pairs of homologous chromosomes the 22 autosomes. The allosome pair of chromosomes is not considert homologous but either "homozygot / homogametic"[XX] or "hemizygot/ hemigametic"[XY].


Well, according to this source there are no flightless bats, so it isn't an absolute that all flying clades have flightless members:

https://pterosaurheresies.wordpress.com/2011/07/21/meet-the-first-flightless-pterosaur-sos-2428/

  Everyone knows about the various flightless birds: the penguin, the dodo, the ostrich… the list goes on. There are no flightless bats. And no one has ever discovered a flightless pterosaur… until now.

But the short answer to your question is: no confirmed flightless pterosaur fossil seems to have been discovered so far.

The longer answer is: from what I can tell no pterosaur has been found that was clearly flightless, but pterosaur flight isn't well-understood in the first place so there is debate as to how and whether some specimens could have flown. It seems to be the consensus so far that they did fly however (based on the lack of mention of flightlessness on the Wikipedia page, and the last paper I link to in this answer is fairly convincing).

As far as not finding flightless specimen, the above link claims to have found one but the source is not reputable and I found no confirmation of it elsewhere (Wikipedia confirms, and I'm usually all about Wikipedia but here the page has all the hallmarks of having been written by the same person who wrote the blog). The same author argues a large pterosaur is flightless here, but their arguments are quite poor compared to others made in the field and they seem again to be the only ones making them.

Here is a post from Tetrapod Zoology in 2008 imagining what a flightless pterosaur might be like, and also claiming none have been found:

  Long-time readers will know that I am an unashamed fan of both speculative zoology, and of Dougal Dixon’s hypothetical ‘alternative’ animals. Inspired by a comment made here in August by Jenny Islander, I have been having a re-think about the possible evolution of flightless pterosaurs: the fossil record gives no indication that such animals ever existed, and maybe they didn’t, but that hasn’t stopped people from speculating.

A similar quote from the 2004 book "Posture, Locomotion, and Paleoecology of Pterosaurs":

  So far, there is no example of flightless pterosaurs.

The Wikipedia page for pterosaurs makes it clear how hard it is to figure out how pterosaurs flew.

Here is one of the main arguments that the largest pterosaur Quetzalcoatlus northropi was flightless

  The estimated mass for the largest pterosaur known, Quetzalcoatlus northropi, exceeds the previous highest estimates by more than 100%, and it is argued that this extremely large pterosaur is better interpreted as a secondarily flightless form.

And an argument that the largest pterosaurs would have been flightless based on a comparison to modern oceangoing birds:

  Our result therefore casts doubt on the flying ability of large, extinct pterosaurs. The largest extant soarer, the wandering albatross, weighs about 12 kg, which might be a pragmatic limit to maintain a safety margin for sustainable flight and to survive in a variable environment.

This paper summarizes the debates and argues against those assessments (the whole paper is worth reading actually):

  While the conclusions on giant pterosaur flight by Chatterjee and Templin [19], Sato et al. [17], Henderson [25] and other workers using avian analogues for pterosaurs are not without merit, we find that they leave themselves open to criticism by not considering alternative data sources when making inferences about the palaeobiology of extinct animals. Giant pterosaur anatomy, functional morphology and, in the case of Pteranodon at least, sedimentary context all indicate that they were flighted animals and, likewise, clear anatomical distinctions between birds and pterosaurs indicate that only basic mechanical details can be treated interchangeably.


Relationship between genetic diversity within and between species

Metrics of interest
The two metrics you are interested in are

$\pi$ - the mean number of differences between two randomly sampled (with replacement) alleles in a population
$d$ - the mean number of differences between two randomly sampled (with replacement) alleles coming from two different species

Consider two sequences

ATCGTCAAT
ATAGTTAAT

There are 2 pairwise differences between these two sequences (positions 3 and 6).
The whole point here is to understand that two individuals in the same population coalesce at a given time in the past just like two individuals coming from two different species. The number of pairwise differences is just equal to the rate at which mutations accumulate multiplied by the coalescence time. Let me develop this idea with a few equations below.
Neutral Expectations
Let's do the math! We will do two important assumptions below.

Every mutation makes a new allele (it is an infinite allele model)
All mutations are substitutions (no indels, no gene duplication, etc...)

Intro to Coalescence Theory
Let's first make sure you understand the concept of coalescence. Imagine you were to look at an evolving population backward in time. A coalescent event, is an event by which two lineages become one (looking backward in time). For simplicity consider a case of an asexual population (but future calculations don't do this assumption). In an asexual population, two siblings coalesced the previous generation, as in the previous generation the genes they are carrying were in a single individual (their parent).
We will see below how to calculate coalescence time between two randomly drawn individual from a population and how we can make inference about genetic diversity from this coalescent time.
Rate of accumulation of neutral mutations
The rate of accumulation of neutral mutation is also called the fixation rate of neutral mutations. Let $fix$ be this fixation rate. Consider a panmictic diploid population of constant size $N$. At a given locus of interest, the mutation rate is $\mu$. The number of mutations occurring every generation in this population is $2N\mu$ (The $2$ comes from the fact that in a diploid population, there are two homologous copies of every gene in each cell). If the mutation is neutral, then every single individual in the population has the same probability to end up being the parent of the whole population in a long time in the future. In other words, starting to look at this problem from the future and looking backward in time, any individual in a distance far enough in the future descends from a single individual in the present. As a consequence, the probability of a new mutation to reach fixation is $\frac{1}{2N}$. Multiplying the probability of fixation by the rate at which mutations occur in the whole population we obtain $\frac{1}{2N} 2N\mu = \mu$. In other words the rate of fixation of new neutral mutations is simply equal to the rate at which mutation occur.
Key equation:
$$fix=\frac{1}{2N} 2N\mu = \mu$$
$d$ - number of pairwise differences between randomly sampled (with replacement) alleles coming from different species
Consider two species which common ancestor lived $T$ generations ago. Each lineage accumulated mutations at rate $\mu$ (and explained above) and therefore the expected (average) total number of pairwise differences is $\bar d=2\mu T$. The probability of having exactly $d$ pairwise differences comes from a Poisson distribution with rate $2\mu T$ ($P(D=d) = Poisson(2\mu T)$).
Key equation: $$\bar d=2\mu T$$
$\pi$ - number of pairwise differences between randomly sampled (with replacement) alleles coming from the same population
Here the calculations follows the same logic as above $\pi = 2 \mu T$. The whole issue is that $T$ (the coalescence time) is unknown for the moment and we need to calculate it.
Let $P(T)$ be the probability that two randomly sampled (with replacement) individuals from a diploid panmictic population coalesce exactly $T$ generations ago. The probability of coalescing in a given generation is simply the probability for drawing the same individual, that is $\frac{1}{2N}$ and the probability of not coalescing in any subsequent generation is $1-\frac{1}{2N}$. Iterating over the generations we obtain
$$P(T) = \frac{1}{2N} \left( 1-\frac{1}{2N} \right)^T \approx \frac{1}{2N}e^{-\frac{T}{2N}}$$
, where $e \approx 2.7$ is Euler's number. The above approximation is accurate for large $N$ (say larger than 100). In case you are interest, you will find on this Math.SE post, an explanation for this approximation.
The expected value (average) $\bar T$ of this distribution is $\bar T=2N$ (and the variance is $var(T) = 4N^2$). As a consequence the expected number of pairwise differences between these two individuals is $\pi = 2 \mu 2 N = 4N\mu$
Quickly speaking, these calculations can be extended to calculate the coalescent time between $k$ randomly sampled alleles. The expected coalescent time is then $\bar T = \frac{4N}{k(k-1)}$ and therefore some algebra shows that the total expected time (along all branches) is $4 N \sum_{i=1}^{k-1}\frac{1}{i}$ and the expected number of segregating sites is $4 N \mu \sum_{i=1}^{k-1}\frac{1}{i}$.
Key equation: $$\pi = 4N\mu$$
Conclusion
It is clear from the above that $\pi = 4N\mu$ and $d=2\mu T$ are correlated as they are both linearly related to the mutation rate. As it is said in your quote

For neutral mutations, a positive association between $\pi$ and $d$ should exist, because the neutral theory predicts that both quantities are linearly proportional to the rate at which neutral mutations arise

The quote goes one saying

Recent genome-scale data shows instead that this association is in fact negative.

Such negative relationship between $d$ and $\pi$ cannot be caused by neutral processes. Therefore selection must be involved somehow.
Imagine for example that two species are both selected at different optima (opposite selection pressures). In such case, you would see purifying selection within species reducing the probability of a new mutation to reach fixation to a value lower than $\frac{1}{2N}$ and therefore reducing the rate of fixation $fix$ so that $fix<\mu$. However, such opposite selection pressure among species will yield the species to diverge more than expected by random processes that is $\pi > 4N\mu$. Such selective pattern could explain the observed negative relationship.
More information
This post offers book recommendation on the subject (population genetics).