How does heart beat faster while doing a strenuous task? I know that when we do tasks which require extra physical effort (like running etc.), our heart beats faster.

I also know that the reason behind this is that these jobs require more energy than usual and, hence, require more oxygen for breaking down food. And, since, oxygen is transported throughout body by blood (by forming compound with Haemoglobin (present in RBCs), called Oxyhaemoglobin), the heart needs to beat faster to pump more blood.

However, I am not aware of how does the heart automatically start beating faster.

Is there any involvement of the Nervous System?
Does the heart have some sort of special mechanism that activates when the body performs a strenuous job?

I am sure that there are many ways that your body can regulate heart rate, but I am going to cover this topic briefly from the perspective of $\ce{CO2}$/$\ce{O2}$ concentrations, and pH.

The medulla oblongata

The medulla oblongata is part of the central nervous system, and makes up the lower portion of the brain stem. It is responsible for performing autonomic functions, including the regulation of heart rate through chemoreceptors. The medulla oblongata receives its blood supply from the vertebral artery and makes both afferent and efferent connections with the vagus nerve.

Chemoreceptors

There are two main types of chemoreceptors in your cells that are responsible for regulating heart rate.

Central chemoreceptors

These are located in the medulla oblongata, and are responsible for measuring the concentration of $\ce{H+}$ ions (ie. pH). When the pH is low, neural cells with these receptors will signal the release of norepinephrine and epinephrine.

Peripheral chemoreceptors

These are located in the carotid and aortic bodies and measure the concentration of $\ce{O2}$. The receptor cells of these structures make connection with afferent nerves, to send a signal to the central nervous system in times of hypoxemia.

$\ce{CO2}$/$\ce{O2}$ Exchange

Blood is the tissue responsible for distributing chemicals around your body. It is therefore also involved in the $\ce{CO2}$/$\ce{O2}$ exchange between tissues. Blood cells use hemoglobin as as a carrier molecule for this exchange.

When $\ce{O2}$ is delivered to tissues, it will be processed by the mitochondria of the cells to synthesise ATP, and $\ce{CO2}$ as a biproduct. ATP is also responsible for muscle contractions, and so, with exercise comes an increased utilisation of ATP. With ATP stores running low, your cells will begin to use more $\ce{O2}$, and therefore, they will produce more $\ce{CO2}$.

$\ce{CO2}$ and Acidity

So, I kinda lied when I said hemoglobin is the carrier of $\ce{CO2}$. This is mostly true, but $\ce{CO2}/$$\ce{O2}$ is also somewhat soluble in blood, and this accounts for changes in blood-pH.

$\ce{CO2 + H2O}$ $\ce{<=>}$ $\ce{H2CO3}$ $\ce{<=>}$ $\ce{HCO3- + H+}$

The above equilibrium is catalysed by carbonic anhydrase, and accounts for a decrease in pH levels.

Signalling in response to pH

So your exercising, your body is using lots of $\ce{O2}$ to produce ATP. Your $\ce{CO2}$ levels have increased, and your internal pH has dropped. Now what?

Well, as I'm sure you have guessed, your nervous system takes over.

The central chemoreceptors of the medulla oblongata send an impulse to  the adrenal glands in response to the decreased pH. This signals the release of the hormones epinephrine and norepinephrine in to the bloodstream. The release of epinephrine and norepinephrine is regulated by the sympathetic nervous system. This accelerates the heart rate by binding β-receptors in your heart tissue. Efferent nerve connections from the vagus nerve also participate in this process (I think).

For mechanisms on heart contration, see here; everything following "excitation contraction coupling" is probably the most relevant.

In short, whenever there is role of controlling mechanism, neural and humoral used to get involve. Paraventricular nucleus of hypothalamus controlling the medulla autonomic nervous system. While resting vagal tone is inhibited, sympathetic predominates leading to positive chronotropic and inotropic effect. Emotional and other factor also involve. Even anticipatory effort can have the effect. Humoral is through hypothalamo-hypophisial-adrenal medullary axis.


What insect is this? (India) Can anyone tell me what kind of insect (if it is one) is this...!! Or is it the pupa of some insect?

Well I don't think that the whole big thing is the insect itself, it appears to be just a kind of protection or shelter which moves along with the tiny little thing that keeps on popping out and going it so as to move.
Location:  India

This is mostly a guess and loose suggestion, since the picture is not very clear (would need to see the larvae in more detail). However, Bagworm moths (Psychidae), Case moths (Coleophoridae) and Caddisfly larvae (Trichoptera, almost exclusively aquatic) all build similar cases. They construct their cases out if silk and often include debris, pebbles and other materials. I wouldn't be surprised if the larvae in your picture belongs to one of the first two taxa. Bagworm moths and Caddisflies generally include lots of external materials in their larval cases, which could point to Case moths for your specimen (which seems to have a weaker case mostly made of silk).

Here are two pictures of first a UK Case moth larvae (Coleophora deauratella) followed by a Bagworm moth (Dahlica triquetrella), just as comparisons. If you do google image searches of "group name + larvae" you will see many examples of what they can look like.

And just as a cool example - the larvae often use random material lying around to build their cases, which can give the following result, if caddisfly larvae are bred in a tank containing pieces if gold and pearls. For further information see this link.

It's a household casebearer, a kind of moth larva in the family Tineidae that builds this case around itself.

@fileunderwater is wrong


Why don't antibodies generally bind to food and drugs? Are these excluded thru central tolerance?  What if you ingested something with a unique molecular structure that you hadn't ingested before?

B cells containing receptors against food's or drug's molecular structures may exists. However if the naive B cell binds the molecule without a second signal coming simultaneously from CD4 Tfh cells (linked recognition) the B cells recognizing this antigen will become anergic or will die by apoptosis. This occurs with antigens to which we are chronically exposed, like food.

Reference: Janeway's Immunobiology, 8th edition. Chapter 8 (The development and survival of lymphocytes). In particular section 8-26, p320-321.

I’m not an immunologist, but I think it fair to say that antibodies may well be able to bind to certain food or drugs. However there are several reasons that this may not cause their removal or trigger an immune response. These include:

Location. If the food is in the stomach I imagine that the digestive environment favours breakdown to sugars, amino acids etc and exposure to antibodies is minimal.
Chemistry. Certain substances such as fat, nucleic acids, are weakly antigenic.
Size. Small molecules are not immunogenic unless attached to a larger one.

Why are small molecules not immunogenic?

I think this is probably the key point here, so I'll expand on it a little in general terms.

If an antibody binds a foreign protein, this is large enough that other antibody molecules can bind it too. And the antibody is bivalent, so it may bind a second foreign protein. This leads to a cross-linked matrix that can be recognized by macrophages and engulfed. If a small molecule binds to an antibody this cannot happen and the molecule may well diffuse off again.

As well as binding those soluble antibodies (IgG) already present, antigens cause the antibody-producing cells (B-cells) to divide to produce more of the particular antibody. This happens because the B-cells have a membrane bound variant (IgM) with the same specificity on their surface. When a molecule binds to two of these membrane antibodies a signal is triggered to the cell. This can happen with a large molecule, but a small molecule can bind only one IgM on the surface and this expansion of antibody-producing cells will not happen.

This size requirement for immunogenicity can be understood in the context of the size of the bacteria and viruses which one presumes the immune system evolved to combat.

More Information

As I mentioned, I deliberately answering the question in general terms. If you wish to know more detail (and about cellular immunity) the following on-line book chapters (although a little out of date) may be of interest.

Berg et al. Ch. 33
Alberts et al. Ch. 24


Loss of function in inflammation The Wikipedia-article about Inflammation says

  The five classical signs of inflammation are heat, pain, redness, swelling, and loss of function (Latin calor, dolor, rubor, tumor, and functio laesa).

What does 'loss of function' mean? And how does it occur?

TL;DR: It originally referred to abnormality in "secretion" by the inflamed tissue and later became used to mean any abnormality at all.

This fifth cardinal symptom of inflammation seems to be rather mythological as laid out in detail by Rather (1971, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1749862/?page=3). This source explains that the term seems to have been invented at some point in the 19th century without proper definition. Later authors seem to have interpreted it as basically just meaning "not functioning properly" (although this is literally the definition of unhealthy as opposed to healthy, and not specific to inflammation).

According to Rather, the original source of the confusion may have been the phrase: "...heat, redness, tumour and pain; to which should be added an alteration or suspension of the natural secretions of the part." by Macartney in 1838 (page 8 of the same document). Various versions of mentioning a fifth cardinal symptom that involved altered function made their way through pieces of writing, until it received the Latin term "functio laesa" in the late 19th century (Rather cites a piece from 1882), lending it credibility as an established concept. The passage by Macartney was later cited by Marchand in 1924, who was trying to clear up the confusion around who established the four and potentialy fifth cardinal symptoms of inflammation. Marchand rephrased it into a "fifth cardinal symptom the alteration or disappearance of normal secretion (thus a functio laesa)", trying to explain what, according to Macartney, is the fifth symptom, and adding why it could be called a "loss of function".

Usually, loss of function means some sort of limitation in physical performance. Either force, range of motion, or some other aspect of movement. In this context, loss of function can occur by at least two mechanisms:

mechanical loss of function due to swelling of the tissue around the joint
limitation due to pain associated with movement, part of movement, or too high load.


What is the difference between sinew and tendon? I wonder what the difference between sinew and tendon is. I searched for it but didn't get any clear answer:

https://www.quora.com/Whats-the-difference-between-sinew-and-tendon:

  They are often used interchangably but to be technical, a tendon
  connects a muscle to a bone. The term sinew also seems to include
  ligaments which connect bones to bones. It is however, not a medical
  term.

https://answers.yahoo.com/question/index?qid=20070410182936AA2Kcnk

  Sinew is another word for muscle which is the functional unit of
  movement.

  Tendons connect bone to muscle to make movement possible: The muscle
  contracts and pulls the bone that it's connected to Source(s)

http://the-difference-between.com/tendon/sinew :

  Sinew is a synonym of tendon. As nouns the difference between sinew
  and tendon is that sinew is (anatomy) a cord or tendon of the body
  while tendon is (anatomy) a tough band of inelastic fibrous tissue
  that connects a muscle with its bony attachment.

http://www.thefreedictionary.com/sinew

  sinew = tendon

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

  A tendon (or sinew) is a [...]

Is sinew a synonym for tendon, and if not what is the difference?

They get used somewhat interchangeably, which blurs the lines on the definitions.

When I had my anatomy classes, sinews were regarded as an inclusive class, which included both ligaments and tendons.

For the breakdown:

Tendon: Fibrous tissue that connects muscle to bone.
Ligament: Fibrous tissue that connects bone to bone.
Sinew: Includes both of the above.

A tendon is a fibrous connective tissue which attaches muscle to bone. Tendons may also attach muscles to structures such as the eyeball. A tendon serves to move the bone or structure. A ligament is a fibrous connective tissue which attaches bone to bone, and usually serves to hold structures together and keep them stable. So sinew = tendon. Sinew is a bit more general and somewhat ambiguous. It is mostly used today synonymously with tendon, but historically it has been used to mean either tendons or ligaments, or even to mean muscle.


What percentage of the genetic variance is explained by the 'n'- most important loci? Introduction
Standard models in population genetics look up at the evolution of few loci which impact fitness. The variance in fitness is determined by the genetic variance and the environmental variance (and the co-variance between environment and genetics). In this question I am interested only about genetic variance and about what percentage of the total (additive or not) genetic variance in fitness do 'n' loci explain.
Question
In general, in natural populations, what percentage of the total genetic variance is explained by the 'n'- most important loci?
Here, by "most important loci" I mean loci which variance explain much of the total genetic variance.
In other words, the subquestions are of the kind:

how much of the fitness variance does the most important locus explain?
How much of the fitness variance do the 3 most important loci explain?
How much of the fitness variance do the 100 most important loci explain?

Of course, the answer depends on the population under consideration. Factors that might influence the answers are for example

species
population size
environment stability
…

Beside this question, I also welcome some insights concerning how different factors are likely to influence the answer.

From the statistical point of view, this question is rather vague. One would need a mathematical definition for the term "genetic variance".

In one extreme, if the "genetic variance" merely means the categorial variations of nucleotides (i.e. ACTG) in the pooled genomes of interest, then the distribution of total "genetic variance" vs. loci variation is uniform and only depends on the size of the locus.

In another extreme (among many dimensions of extremes), if the "genetic variance" is only manifest by the organism's immediate "fitness" and only has two values: life and death (on birth), then all the "essential genes" are "the most important" loci. If you're interested in the n most important loci where n > the number of essential genes, then you would first look at the binary genetic interactions in the database such as BioGrid where two non-essential genes would "interact" and change the organism's fitness (in life and death).

Of course none of the two extremes is very interesting in population genetics or evolution, but a statistical question is best phrased by statistical terms. I would try to find the mathematical definition for "fitness variance", too.

---EDIT---

For a semi-empirical/informatics study, I think you could start with the simplest organism whose genome is well studied.

Choose an organism (e.g. yeast)
Assume uniform inheritability
Choose a specific measurable phenotype/environment (e.g. the ability to grow on a specific sugar x)
Scan each gene in the yeast genome and see its quantitative impact on growth (They're documented in various database)
Ignore genetic interaction
(Or scan each gene pair/triplet/.../n-cluster to see its impact on growth on x)
Try to model your empirical distribution. It's only valid for that specific phenotype/environment
Define your "TOTAL genetic variance in fitness" meaningfully and rigorously. "Additivity" would be a very drastic assumption.

My guess as a non-geneticist is that, as rg255 suggested, for each phenotype as a function of the environment, the distribution would follow a power law. They would not have the properties that would allow you to use central limit theorem to "add them up". But for a specific phenotype, your empirical cumulative distribution function (cdf) would answer your question.


Why didn't the polar bear change its color from white to black during evolution to absorb heat? Polar bears are white in color and white color is not a good absorbant of heat. Why then didn't they evolve a black color to absorb more heat?

Polar bears do not have white fur - they don't have pigments in their fur hairs which makes them clear and translucent. The outer fur consists of hollow fibres, which shatter a part of the incoming light (the visible part) which makes them look white. This gives a very good camouflage in a white environment.

It was initially thought (see reference 1) that the hollow fibers work in the same way as fiber optic cables and direct the UV part of the light (the visible was thought to be shattered) towards the black skin of the bears where it generates heat, but this hypothesis has been disproved. The UV part of the light is simply absorbed by the bears outer fur and doesn't reach the skin (see reference 2 for details).

The hollow hair helps with the insulation of the skin and can change the color due to environmental influences. The tend to get yellow after feeding on seals due to the fatty substances from the animals. There have also been reports from zoos that algae lived inside the hollow part of the fur making the animals more grey and sometimes even green (see reference 3).

Reference:

Light collection and solar sensing through the polar bear pelt
Is polar bear hair fiber optic?
The greening of polar bears in zoos

Well, Polar bears do have black skin; But, living in the harsh arctic conditions they've adapted several traits such as thick layer of blubber, wide paws etc. But their most peculiar trait is having a white fur coat; unlike other bears, polar bears have evolved to have white fur with hollow hairs which easily allows their black skin to absorb the radiations from the sun. So there's no problem with the heat intake.

Now, the reason behind their white fur lies in their quest to food. The white fur enables them to easily hide/blanket in their surrounding (the white masses of snow) i.e. it helps them in camouflage.

And, I guess that's it! Thanks!


Why do our eyes close when we sleep? Why do our eyes close when we sleep? Is it to relax our eye muscles? How can it be explained from an evolutionary point of view?

Our eyelids close when we sleep probably for the obvious reason that it prevents the sclera and cornea from drying out, becoming accidentally scratched (such as blowing dust) and allowing oxygen diffusion from the inside of the eyelid (to the sclera and cornea). Fragile corneas are a requirement for our vision. Thick corneas are much less fragile but then attenuates more light.

From terdon:

1) blinking requires muscle movement which sort of defeats the purpose of resting

2) closed eyelids offer much better protection than periodic blinking

3) if you can blink, you have eyelids.

Tears contain an important hormone that kills bacteria. Closing eyelids during sleep allows a prolonged contact between the cornea and tears killing resistant bacteria in the process. The action of the tears during blinking is not sufficient to completely get rid of the foreign bodies in the eyes. Closing eyelids gives the tears a capacity to accumulate forming a film of moisture above the cornea and acqeous humour. This has many important uses. It allows dust particles to dissolve and be eradicated when the tears flow out of the eyelids. This partially explains the residue that is seen on the cheeks when people wake up in the morning in addition, of course, to the sodium and potassium salts in the tears. The other importance of the film of tears accumulated on the eye is to help keep the acqeous humour moist. This has a great effect on how the lens receive light and also on the overall refractive index  of the eye as system.


Why doesn't our immune system react to infused antibodies produced in a horse? Calmette tried injecting horses with snake venom and then taking out the serum which has produced antibodies against the venom and injecting in the snake-bitten human.

Shouldn't our immune system recognize this exogenous protein and try to eliminate it as it's a non-self protein?

Our immune system does react to horse antibodies, but as with any adaptive immune response it takes some time for the response to develop. In the weeks before our immune response fully responds to the horse antibodies, the infused antibodies can have their effect.

If you then have a second infusion of horse antibodies, the immune response would not only prevent them from having their beneficial effect, but it might case serious adverse effects.  This serum sickness (Wikipedia link) has been known for over a century; here is a paper from 1918 discussing it as a well-known issue:

  The injection of horse serum either in small or in large amounts in human beings is always followed sooner or later by the development of hypersensitiveness of the skin to subsequent injections of horse serum. For the development of this reaction serum disease is not essential.

--THE RELATION OF CIRCULATING ANTIBODIES TO SERUM DISEASE. J. Exp. Med. Published March 1, 1918

Although there aren't many modern situations in which horse (or other non-human species) serum is injected into humans, when it is (as with anti-venom, which is generally produced in non-human animals) serum sickness is still a concern.

  Serum sickness is a delayed immune reaction resulting from the injection of foreign protein or serum. Antivenom is known to cause serum sickness but the incidence and characteristics are poorly defined. ... The primary outcome was the proportion with serum sickness, pre-defined as three or more of: fever, erythematous rash/urticaria, myalgia/arthralgia, headache, malaise, nausea/vomiting 5–20 days post-antivenom.

--Incidence of serum sickness after the administration of Australian snake antivenom (ASP-22). Clinical Toxicology. Published  2016

Human/mammalian immune system do not react to everything foreign that enters the body. This foreign substances are called "antigens". Instead, the host [i.e. body] reacts to "immunogens" - these are antigens, that CAN elicit immune reaction. Microbes are immunogens, for instance. They don't only consist of microbe proteins, but also of so-called PAMPs, pathogen-associated microbial particles. This can be a bacterial cell wall or "peculiar" DNA and double-stranded RNA, that are definitely cannot be found in mammalian tissue. And these PAMPs are recognized by PRRs, pattern recognition receptors, that are found on innate immune cells, such as dendritic cells and macrophages. WITHOUT activation of innate immune cells, without, basically, INFLAMMATION, the overall immune reaction is not possible. At least, this is a current concept.

So, horse antibodies are not sufficient to elicit immune reaction.
In order to induce immune reaction, these antibodies should be injected with something, that can activate PRRs or cause tissue damage, like aluminum dioxide. The latter substance is largely used in formulation of vaccines. Guess, why ;-)

Of course, there are immune reactions to proteins or harmless xeno-antibodies, but this is usually not physiological, if the manifested reaction is severe. Example: food allergy to egg protein, ovalbumin.

Hope, it helped.

Best,
S


Steroid hormones: how do they travel through the cytoplasm (not just the blood plasma) if they're hydrophobic? I get that steroid hormones need hydrophilic plasma protein carriers (eg albumin, TBG) to travel in the plasma because they're not soluble in the plasma. However, I don't see any sources talking about how these hormones can then traverse through the (presumably also hydrophilic) cytoplasm to get to their receptors either in the cytoplasm or nucleoplasm. Anyone have any clarifications on this?

Firstly not all steroid hormones travel inside the cell and regulate the gene expression.
Basically there are two pathways- direct and indirect.
Steroid hormones are lipid-soluble, which allows them to cross the extracellular membrane to the inside of the cell.

Classical models of steroid action suggest that steroid hormones bind to specific nuclear receptor proteins once inside the cell. Reference

Once inside the cell, a steroid hormone binds with receptor proteins in the cytoplasm. The steroid hormone and its receptor form a complex, called a steroid complex, which moves into the nucleus where it influences the expression of genes.
Reference

In the indirect pathway,

The traditional nuclear steroid receptors can also indirectly regulate gene transcription by serving as signal transduction proteins that interact with various signaling pathways in the cytoplasm of a cell. In particular, ER can activate kinases, enzymes that phosphorylate and thereby activate other proteins. This sets in motion a signaling cascade that eventually ends in the nucleus with the induction of gene transcription.
Reference

I suspect the issue is mainly one of diffusion distance. Steroid hormones are not that insoluble as they are compact and have multiple oxygen functional groups. Checking predicted log octanol/water partition coefficients on PubChem gives 3-4ish for steroid hormones compared to 6+ for a typical fatty acid, despite the latter having an ionizable headgroup.
These hormones are present in the body at nanomolar concentrations or even lower, and at that concentration, almost anything is soluble. The problem with them being in the plasma at any concentration, though, is that as soon as a molecule would collide with the lipid membrane of a cell in the wall of the vessel, it would tend to stick, and therefore the vessels would act sort of like a chromatography column that drastically reduces the apparent diffusion coefficient and generates steep gradients. While this might actually be desirable for a local mediator like a prostaglandin that has a range of a few cell diameters, it is very undesirable for something like steroid hormones that travel to completely different organs from where they are produced. Therefore, a hydrophilic carrier is essential.
On the scale of the cytoplasm of a single cell, this is not likely to be an issue, especially since there are receptors inside that act as a "sponge" or "sink" to catch and trap molecules that diffuse in.


Virus viability on fabrics According to the article How long do viruses live on surfaces: Plastic, stainless steel, fabric, and more:

  With fabrics, it's unclear how long viruses can last. But generally, they tend to last for a shorter amount of time on fabric compared to hard surfaces like stainless steel, according to the Mayo Clinic.

Can someone kindly explain why this is so?

What is it about fabrics that decreases virus viability?

I would like to point out here that in many cultures our ancestors had figured it out empirically.  In North India, where I hail from, many old people will eat bread, snacks etc. from a cloth (especially a woolen fabric) if their hands are dirty.  The simplistic explanation given is that this type of fabric "stays pure".

A VERY interesting question that I had to think a lot about, and frankly I couldn't come up with an answer.

Nevertheless, this article may have.

https://www.statnews.com/2020/03/19/coronavirus-survives-on-surfaces-how-to-protect-yourself/

"Viruses covered in “envelopes” have the most trouble surviving outside a living cell. On surfaces, the surrounding light, heat, and dryness break down the envelope, killing the virus. (Porous surfaces pull moisture away from viruses that land on them, accelerating the destruction of the envelope.) Most rhinoviruses have such envelopes; so do some influenza viruses. Norovirus doesn’t, enabling it to last longer in the environment."

Here are the author's relevant credentials.

Sharon Begley, senior science writer, covers genetics, cancer, neuroscience, and other fields of basic biomedical research. She was previously the senior health and science correspondent at Reuters, the science columnist at the Wall Street Journal, and the science editor at Newsweek. Among her favorite awards are an honorary doctorate from the University of North Carolina and the Public Understanding of Science Award from the Exploratorium in San Francisco.


What is a function-triggering antibody? I am reading a journal paper on the effect of a neural cell adhesion molecule on neuronal development and in the abstract of this paper I have come across the following:

The autophosphorylation and activity of Pak1 were enhanced when
isolated growth cones were incubated with NCAM function triggering
antibodies, which mimic the interaction between NCAM and its
extracellular ligands.

In this paper, the NCAM protein becomes activated when it is exposed to NCAM function triggering antibodies. I understand that antibodies are molecules produced by the immune system and bind to antigens. However, I am not sure how incubating growth cones with NCAM triggering antibodies would actually trigger/activate the NCAM protein itself.
Isn't the purpose of an antibody to bind to an antigen  so that it can be removed from the body? I am not sure how exposing an antigen its respective antibody would trigger its function. I have read several other papers about neural cell adhesion molecules where antibodies were used to activate their function. I have searched function-triggering antibodies on Google but I have found no useful results regarding this. Any insights are appreciated.

The term "function-triggering antibodies" is not standard, these are more widely known as cross-linking antibodies. As you may know, an antibody has multiple "arms", with the antigen binding region or Fab (Fragment antigen binding) at the end. IgG antibodies have 2 arms, IgM can have 10. The Fab portion is generally identical on all the arms, although it's possible to engineer them differently. This allows the antibody to bind to multiple antigens at the same time, drawing them close together.
NCAM is a homophilic binding protein, with an extracellular domain that binds to other NCAM molecules, both on neighboring cells and on the same cell. That binding induces structural changes in the intracellular domain which promotes the binding and activation of kinases, proteins that phosphorylate (and thus activate or inhibit) other proteins. This starts a signaling cascade that induces changes in the cell, typically by controlling the activity of transcription factors in the nucleus.
Receptors are generally not spread out evenly over the surface of the cell, they often exist grouped together in membrane structures known as lipid rafts. When drawn close enough together, NCAM molecules can begin their signaling cascades on their own, as adapter proteins bound or recruited to the intracellular domains get activated – the kinases and their substrates are in close proximity as well. To induce this type of signaling in the lab, cells can be treated with cross-linking antibodies that draw the receptors together. This in effect triggers the function of the receptors, beginning their downstream signaling.

Source

Antibodies can function as enzymes (see https://en.wikipedia.org/wiki/Abzyme).
If you use the right monoclonal antibody, the variable end can be the right shape to bind to the site you mention.


Why do only two sexes exist for animals? Why, from the natural selection point of view, do only two sexes exist for animals?

To get a non-circular answer to why humans and other mammals have only two sexes, it's helpful to take a look at our evolutionary history.  While mammals possess several adaptations to a terrestrial life cycle, including internal fertilization and gestation, which require substantial anatomic specialization between males and females, these are all secondary features that evolved long after our aquatic ancestors had acquired two distinct sexes.

Indeed, if we look at animals like fish, which reproduce via external fertilization, it's not at all obvious why they might not have more than two sexes.  After all, for many aquatic animals, mating involves little more than the female and the male releasing their respective gametes into the water, where they meet and fuse to a form new zygote, which can then divide and grow into a new adult.  Seen that way, there seems to be no reason why there could not be more than two "mating types", as in many fungi, such that gametes of any two distinct types could fuse into zygote.

The answer lies in the fact that the male and female gametes aren't actually that similar: the female gametes, or eggs, are typically large cells that contain all the nutrients necessary for the new zygote to develop into a viable individual, whereas the male gametes, or sperm, are tiny and produced in huge numbers.  This asymmetry is known as anisogamy, and modeling its origin has been an important topic in the theoretical study of evolution.

Without going into details on the evolution of anisogamy, once it exists, it clearly forces the mating types to also split into two groups: there's no advantage in two microgametes (sperm) fusing, since the resulting zygote would lack the nutrients it needs to be viable, whereas the fusion of two macrogametes (eggs) would simply be inefficient — eggs, being large, are comparatively rare and expensive, and wasting two of them to produce only one offspring would be suboptimal even if the resulting zygote was viable.  Nor is there really room in such a scheme for gametes of intermediate size: they'd be too small to fuse into a viable zygote with sperm, but too large to be produced in sufficient amounts to be effective in fertilizing eggs.

Of course, there's nothing that would stop a single adult from producing both micro- and macrogametes, but such an adult would not really be a third sex — it would just be male and female at the same time, a mating strategy known as (simultaneous) hermaphroditism, which indeed occurs relatively often in nature.

So, if pretty much all animals are anisogamous, why do fungi remain isogamous (and often have multiple mating types), then?  Well, one explanation is that the main drivers for the evolution of anisogamy — sperm competition and transportation risk — don't really apply to fungi, which mate when two sessile haploid mycelia grow and come into contact with each other.  Since the gametes are not motile, there's no advantage for either/any sex to produce more of them (at the cost of smaller size) in order to increase the chance of successful mating.  Thus, isogamous mating works fine for the lifestyle of fungi, and having multiple mating types is then a useful adaptation to make successful mating between neighboring mycelia more likely.

The purpose of sexual reproduction is to combine the genetic material from the contributing parents to produce a new individual. That combination has the potential to replace genes which may be defective and generally increase diversity in the offspring, improving resistance to certain pathogens. Bottom line: sexual reproduction confers an evolutionary advantage.

Where it occurs, why only two sexes? Simply because two is sufficient to get the job done.

Consider the perspective of one "parent", and the goal to combine genetic material from some other source of the same species in order to produce an offspring having some blend of genetic material. If that "other source" was one randomly selected individual, how does an additional randomly selected source qualitatively change the result? By the principals of statistics, it doesn't. One other source containing some random variation is no more or less random than a combination of two or more such sources. Therefore, to meet the requirements of a random genetic shuffle, two sexes suffice.

If a third sex was required, then three individuals would have to play their respective roles for successful procreation, where only two are required for the two-sex system we understand. If you compare asexual reproduction with two-sex reproduction, you might wonder why asexual reproduction exists at all given the genetic benefits of sex. The answer is in simplicity. No need to find a partner. To go from two sexes to three, there would have to be a benefit to overwhelm or at least balance the added complexity of bringing three partners together instead of just two. As previously discussed, there isn't any. Even if a three-sex system just happened to occur, it would be out-competed by its simpler two-sex rivals.


In plant species' description, does the leaf length include the lamina and petiole, or only the lamina? The description (partially pasted below) of Ramosmania rodriguesii in Verdcourt (1996) states that the leaves are up to 30 cm long. Does this length include both the lamina and petiole, or only the lamina?

Reference (source of above paragraph):
Verdcourt, B. (1996). Ramosmania rodriguesii Rubiaceae. Curtis's Botanical Magazine, 13(4), 204-209.

According to "Plant Identification Terminology: An Illustrated Glossary" (Harris & Harris, 2001) [my emphases added]:

A leaf is "an expanded, usually photosynthetic organ of a plant"

A lamina is the "expanded portion" of a leaf

A petiole is a "leaf stalk" and a stalk is "the supporting structure of an organ, usually narrower in diameter than the organ."

I know you know the definitions here, but I'm using this as evidence that the petiole is often considered separate from the leaf itself.
I do not know of a flora, key, or guide that uses the petiole as part of the measurement.
Since Kew's Plants of the World Online lists this species as having 30 cm long leaves (and assuming they do not include the petiole as is common practice), I would assume your source likewise is not including the petiole.
Disclaimer: I have never seen Ramosmania rodriguesii, so I can't comment from personal experience/knowledge of this specific species. However, if typical measurement practices have been employed, I assume the petiole is excluded in leaf length measurements.

No it doesn't these days. That description of the leaf excludes the petiole length. 38 including both.


Why and how does complexity usually tend to increase through time? The question of complexity is classic in the very first lectures of evolutionary biology where the teacher usually tries to tell the students that complexity does not necessarily increase and that humans are not more complex than other organisms.

My questions are:

Why does complexity tend to increase through evolutionary time?
What are the different hypotheses to explain this pattern?

When writing "Mass extinction" on google image, we find many graphs displaying the number of families (or other taxa) through evolutionary times with the five mass extinctions. What would it look like to draw such graph replacing the family richness in the y-axis by :

Mean complexity among all living things?
Complexity of the most complex taxon?

I suppose that anyone who wishes to answer to this post will necessarily need to define the words "complexity". He or she might define it in terms of number of genes, number of metabolic pathways, length of DNA sequence, number of cell types, some kind of index taken from information theory. When asking my questions I had in mind a definition close to "number of genes" or "number of metabolic pathways".

This is actually a very interesting yet difficult question to give a single precise answer to. I will try and summarize for you a "meta answer":

Complexity Science Some consider complexity not to be a Biological topic as such, since it is a property that accumulates in non-biological systems e.g. economics, technology, music, language - in fact anything that "evolves" through time. This new field of science is called "Complexity Science" or "Complex Systems" and is primarily a field of mathematics or information theory: Complex systems

Complexity in Biology What I can say is that these kinds of questions have started an almost new field in Biology, called "diversity evolution", here is a very interesting paper: Diversity Evolution.

Defining Complexity You were right to mention Complexity first needs to be defined, and as an early field of science this is where much focus has been recently. There are quite a few definitions but it is perhaps too controversial to list any particulars... HERE is a whole UCL lecture dedicated to defining Complexity!

Topics of Complexity Science I have written enough, so perhaps this lovely diagram of the topics of Complexity Science will be of some help:

Biology arises when some molecules begin copying themselves with a certain amount of error: not too much error, or there would be no heritability; but SOME error, or else there would be no evolution at all. Copying, copying, a few molecules become a multitude, and evolution spreads in all directions, to the more and to the less complex. But when a new level of complexity arises, it usually allows a new size, and a bigger organism can, for instance, eat a smaller organism. Once this level is achieved, it tends to be mantained. Again some copies will lead to smaller lineages, but the big ones have founded a niche that will not disappear by itself (it may take an asteroid). So, looking up close, evolution leads to diversity, not only to higher complexity. But since small complexity already existed, and bigger complexity is something new, we tend to perceive evolution as creating complexity - which is not a false point of view.


Skull mystery on beach The skull was found on a beach on the Sechelt inlet on Canada's pacific coast. A marine environment.

What species is this skull from?

We found a very similar skull on a beach near Richardson Bay, Lasqueti BC. Decided it was a seal skull (locals agreed)
See harbor seal skull: http://www.skullsunlimited.com/record_species.php?id=4726

"Dwarf Sperm Whale" Scientific name: Kogia sima


Why does throat 'burn' when you've got a common cold? Apart from pain when swallowing, there's also a persistent feeling of throat 'burning' in the same area.

What causes it and why does it feel that way?

If you've been sneezing or coughing a lot it is probably micro abrasions in the throat. I don't recognize any other burning sensation.

I guess it is because the throat is sore, thus probably inflammated. Inflammations are hot. Though, I am not a doctor.


Do the majority of fish lack scales on their heads? Based on pictures, it seems to me that a vast majority of fish species that have scales do NOT have scales on their heads.

Is that fact true?

To make this properly answerable:

lets' define a "majority" as >70% of fish species. But frankly, I'm more interested in actual numerical answer than whether it passes some arbitrary threshold or not.
The universe which I'm interested in measuring the percentage are fish species that have "normal" (Cycloid and ctenoid is the technical term, I believe?) scales on their bodies.

If that's not specific enough, you can restrict the universe to species in Actinopterygii (ray-finned) that have scales.

I certainly agree with your general observation, but not being an ichthyologist, I can only offer a partial answer, based on a particular family of fish. Within the family Tripterygiidae, most species lack scales on their head, or have highly modified types of scales. A comparative study of 48 species showed that only 2 have "normal" scales of their head (Jawad, 2005).

  The squamation pattern of the bases of the fins
  varies among species. The head is usually devoid of scales
  except for two species that have squamation with body-
  type scales (Matanui bathytaton (Hardy, 1989) and
  Norfolkia clarkei). Several species have head ctenoid scales
  modified into tiny spicules of different shapes (Acantha-
  nectes rufus Holleman & Buxton, 1993, Apopterygion
  oculus Fricke & Roberts, 1994, Axoclinus carminalis,
  Ceratobregma acanthops, Cremnochorites capensis, Ennea-
  nectes boehlkei Rosenblatt, 1960, Forsterygion malcolmi
  Hardy, 1987, Forsterygion varium (Forster, 1801), Karalepis
  stewarti, Matanui bathytaton, Norfolkia clarkei, Notoclinops
  caerulepunctus Hardy, 1989).

So far, I haven't found a broader comparative study, to support your general question. Someone more knowledge in the area and the literature can perhaps offer a more general answer. This is at least an indication that your observation might be correct.

Reference
Jawad. 2005. Comparative scale morphology and squamation patterns in triplefins (Pisces: Teleostei: Perciformes: Tripterygiidae). Tuhinga 16 (1), 137-168

Based on a lack of written evidence, in searching Google and Google Scholar, I believe fish have scales on their heads, where I'm defining 'scales' as 'solid, protective bony scales' [see below], and I'm assuming the fish heads are covered with solid protective bony Big scales.  I think a lack of scales on fish heads would be a fish fact that wouldn't be too difficult to find.

Some fish lack scales altogether, such as gobies and toadfish:
https://www.slideshare.net/gurya87/types-of-scales-in-fishes-44959366
This wikipedia article mentions scales repeatedly [examples below] but says nothing about a lack of scales on fish heads -https://en.wikipedia.org/wiki/Fish_anatomy

a.  The dermis is covered with overlapping scales.

b.  The dermis of bony fish typically contains relatively little of the connective tissue found in tetrapods. Instead, in most species, it is largely replaced by solid, protective bony scales.

c.  The outer body of many fish is covered with scales,


How does temperature affect photosynthesis? I am doing a lab for biology and my teacher required me to do this virtual lab. However, it does not make sense when seeing the results of the lab. In 30 second trials, it shows that there are 16 bubbles at 10C, 6 bubbles at 25C and 19 at 40C. This should not happen as 25C is near the optimal temperature (at least in respiration) but it shows the opposite.

Is the site wrong or am I wrong?

Site link: http://www.kscience.co.uk/animations/photolab.htm

Constants: 50 Light intensity, full disolved co2, white light color.

Your experiment should look something like this: The effect of temperature on photosynthetic rate of Elodea (pondweed). I assume you used Elodea canadensis for your test. Maybe the plant is already a bit "exhausted" - try to take a different branch. Or maybe it needs more time to get used to the new temperature.


Why do we feel headache after ice cold drink? Whenever we drink ice cold drinks, after a couple of seconds, suddenly we feel intense pain rising from upper nose to forehead. What is reason behind this pain after too cold drink and why it's felt in that particular part of head?

The cold drink causes the blood in blood vessels of gums to freeze. This stimulates nerve endings and causes a sensation in brain.


Why do viruses cause different symptoms? If the sole purpose of a virus is to hijack the nucleus of a cell to replicate, why do we have different symptoms for different viruses?

I can think of the following comming into play:

immune response of the body
destroying tissue of type A is different than destroying tissue of type B
the rate of the destruction --- some (virus, cell) combination are causing more harm than others

Reference:

Why Do Viruses Cause Different Symptoms In Different People? --- talks about how we can have different symptoms for the same virus.

every virus having differ differ spike proteins so they make infection  a particular type of cell ( just like HIV that only bind with CD4 type of receptor) and make effect. another fact is that every virus have different genomic marital so that have different codon and these different codon make different protein and that different proteins make different effect on host cell metabolism that's why different virus having different symptoms.


Where can I find the data on the geographical distribution of the species of Drosophila within various areas of the world? Let X denote an arbitrary geographic area where drosophilas occur in the wild. I will need the answers to the questions of the following type:

  What is the three most occurring species of the genus Drosophila within X?

Where can I find the data on the geographical distribution of Drosophila species within various areas of the Earth?

Source: pinterest.com
I have been unable to find data on a global scale, for now here's a map on the USA.


Are specialized cells considered to have life? A common definition of life, including the one in Biology SE Life requires physical entitites to have the capability of being able to reproduce.

A process defining organisms that grow and adapt to stimuli while
maintaining a state of organization and energy production and being
capable of reproduction.

Under this definition one could think that a specialized cell like a bone cell or a skin cell doesnt have life. But also, a common definition of cell, including the one here in Biology SE says a cell is

the smallest unit of life.

So, my question is, are specialized cells which dont reproduce supposed to have life? This question came up to me thinking of other living organisms which have tissues which seems to be inert and survive hundreds or thousands of years (ie, wood, bones, etc.)

Life is defined in many ways.
Common definitions are usually simplified definitions. Under some definitions it would be "life" under others it would not be. But it doesn't matter. The problem you are having is thinking definitions of life are anything more than artificial categorization. Really there is no difference between living things and the rest of chemistry, or at least there is a smooth gradient connecting them, but we humans can't easily think that way, so we create descriptive but imperfect definitions to help our thought processes. There is a lot of gray area for any definition of life, and you have found one.

The short answer is that Yes, specialized cells are considered to have life, as are sterile ants that serve the colony but do not themselves reproduce. The definitions that are given for life are attempts to characterize a phenomenon that people are already capable of recognizing. Specialized cells arose out of a reproductive process and they do other life-y things like metabolizing. So they are alive.
If the definition given in a book seems to imply that specialized cells aren't alive, then the definition is ill-formulated, misunderstood, or both.


Identify the pink mold infecting refrigerated lemons I made lemon juice 6 month ago.

I just washed the lemon using brush and then cut them into pieces.
Then I put one layer of lemon in the bottle followed by one layer of
sugar
Again one layer of lemon and one layer of sugar.
Then I close the bottle and put it in the refrigerator.

When I opened it, I observed some pink colored mold on the lemon slices.

Can anyone can identify the mold or tell me how to identify it?

PS: in the 6 months, I never opened the bottle. The bottle was clean and I did not add water; just lemon and sugar.

I checked citrus diseases on wikipedia, then "ctrl+f" and typed in "pink mold". The result was Gliocladium roseum which is really a pink mold, but it is hard to find any image of it, where it is on fruits... So this is just a guess. Btw. I think it is rarely possible to identify microorganisms just by checking an image of them.


Can a constitutively active kinase be highly regulated? I am studying the protein kinase GSK3 and I am learning about the regulation of its activity. Many journal papers that I have read have stated that GSK3 is unique because it is a constitutively active kinase, meaning that it is always active and is not activated in response to a specific stimulus/condition. I have read that phosphorylation of GSK3 at specific tyrosine residues only enhances its activity, but the GSK3 itself is always active.
However, many of these papers also talk about the various mechanisms through which the activity of GSK3 is regulated (e.g. through phosphorylation at specific amino acid residues, subcellular localisation, protein complex formation). One paper states the following:

The many functions regulated by GSK3 (through its phosphorylation of
numerous substrates) suggests that the activity of GSK3 must be highly
regulated. Four key mechanisms have been identified that contribute to
regulating the actions of GSK3 in a substrate-specific manner. These include regulation by phosphorylation of GSK3 itself, the subcellular localization of GSK3, the formation of protein complexes containing GSK3, and the phosphorylation state of GSK3 substrates.

I am wondering how is it possible for a kinase to be constitutively active and be highly regulated at the same time? If it is constitutively active, doesn't this imply that it is always active? Any insights are appreciated.

I think you have answered your own question, but yes, the nomenclature is confusing. When they say it is a constitutively active kinase, you are right, it plainly means the enzyme can always phosphorylate other molecules/proteins.
The regulation part is what you have in the review paper you cited. If the kinase is always on but localized in a compartment where there is nothing to phosphorylate, it could be considered "regulated". The same logic applies to the other regulation methods listed.


How could humans have interbred with Neanderthals if we're a different species? To be clear, I'm not doubting that homo sapiens and homo neanderthalensis did interbreed: of that much I'm convinced.

Within the past few years I've seen an upcropping of pop-sci articles discussing the interbreeding between pre-historic species of humans. In everything that I see in these articles, as well as in scientific literature (my college Bio textbook, among others), I see these different humans being referred to as separate species.

This conflicts with my understanding of a species. Given the following definition, wouldn't homo sapiens and homo neanderthalensis be the same species?

  A species is often defined as the largest group of organisms where
  two hybrids are capable of reproducing fertile offspring, typically
  using sexual reproduction.  ~Wikipedia

Is this definition incorrect?
Are the publications using "species" colloquially, as opposed to scientifically?
Is "species" still a poorly defined concept? (see Ring Species)

Thanks!

Short answer
The concept of species is poorly defined and is often misleading. The concepts of lineage and clade / monophyletic group are much more helpful. IMO, the only usefulness of this poorly defined concept that is the "species" is to have a common vocabulary for naming lineages.
Note that Homo neanderthalis is sometimes (although it is rare) called H. sapiens neanderthalis though highlighting that some would consider neanderthals and modern humans as being part of the same species.
Long answer
Are neanderthals and modern humans really considered different species?
Often, yes they are considered as different species, neanderthals being called Homo neanderthalis and modern humans are being called Homo sapiens. However, some authors prefer to call neanderthals Homo sapiens neanderthalis and modern humans Homo sapiens sapiens, putting both lineages in the same species (but different subspecies).
How common were interbreeding between H. sapiens and H. neanderthalis
Please, have a look at @iayork's answer.
The rest of the post is here to highlight that whether you consider H. sapiens and H. neanderthalis to be the same species or not is mainly a matter of personal preference given that the concept of species is mainly arbitrary.
Short history of the concept of species
To my knowledge, the concept of species has first been used in the antiquity. At this time, most people viewed species as fixed entities, unable to change through time and without within-population variance (see Aristotle and Plato's thoughts). For some reason, we stuck to this concept even though it sometimes appears to not be very useful.
Charles Darwin already understood that as he says in On the Origin of Species (see here)

Certainly no clear line of demarcation has as yet been drawn between species and sub-species- that is, the forms which in the opinion of some naturalists come very near to, but do not quite arrive at the rank of species; or, again, between sub-species and well-marked varieties, or between lesser varieties and individual differences. These differences blend into each other in an insensible series; and a series impresses the mind with the idea of an actual passage.

You might also want to have a look at the post Why are there species instead of a continuum of various animals?
Several definitions of species
There are several definitions of species that yield me once again to argue that we should rather forget about this concept and just use the term lineage and use an accurate description of the reproductive barriers or genetic/functional divergence between lineage rather than using this made-up word that is "species".
I will below discuss the most commonly used definition (the one you cite) that is called the Biological species concept.
Problems with the definition you cite

A species is often defined as the largest group of organisms where two hybrids are capable of reproducing fertile offspring, typically using sexual reproduction.

Only applies to species that reproduce sexually
Of course, this definition only applies to lineages that use sexual reproduction. If we were to use this definition for asexual lineages, then every single individual would be its own species.
In practice
In general, everybody refers to this definition when talking about sexual lineages but IMO few people are correctly applying for practical reasons of communicating effectively.
How low the fitness of the hybrids need to be?
One has to arbitrarily define a limit of the minimal fitness (or maximal outbreeding depression) to get an accurate definition. Such boundary can be defined in absolute terms or in relative terms (relative to the fitness of the "parent lineages"). If, the hybrid has a fitness that is 100 times lower than any of the two parent lineages, then would you consider the two parent lineages to belong to the same species?
Type of reproductive isolation
We generally categorize the types of reproductive isolation into post-zygotic and pre-zygotic reproductive isolation (see wiki). There is a lot to say on this subject but let's just focus on two interesting hypothetical cases:

Let's consider two lineages of birds. One lineage has blue feathers while the other has red feathers. They absolutely never interbreed because the blue birds don't like the red and the red birds don't like the blue. But if you artificially fuse their gametes, then you get a viable and fertile offspring. Are they of the same species?

Let's imagine we have two lineages of mosquitoes living in the same geographic region. One flying between 6 pm and 8 pm while the other is flying between 1 am and 3 am. They never see each other. But if they were to meet while flying they would mate together and have viable and fertile offsprings. Are they of the same species?

Under what condition is the hybrids survival and fertility measured
Modern biology can do great stuff! Does it count if the hybrid can't develop in the mother's uterus (let's assume we are talking about mammals) but can develop in some other environment and then become a healthy adult?
Ring species in space
As you said in your question, ring species is another good example as to why the concept of species is not very helpful (see the post Transitivity of Species Definitions). Ensatina eschscholtzii (a salamander; see DeVitt et al. 2011 and other articles from the same group) is a classic example of ring species.
Species transition through time
Many modern lineages cannot interbreed with their ancestors. So, then people might be asking, when exactly did the species change occurred? What generation of parent where part of species A and offspring where part of species B. Of course, there is no such clearly defined time in which transition occurred. It is more a smooth transition from being clearly reproductively isolated (if they were placed to each other) from being clearly the same species.
Practical issue - Renaming lineages
How boring it would be if every time we discover the two species can in some circumstances interbreed, we had to rename them! That would be a mess.
Time
Of course, when we talk about a species we refer to a group of individuals at a given time. However, we don't want to rename the group of individuals of interest every time a single individual die and get born. This notion yield to the question of how long in time can a single species exist. Consider a lineage that has not split for 60,000 years. Was the population 60,000 years ago the same species as the one today? The two groups may differ a lot phenotypically and may actually be reproductively isolated if they were to exist at the same time.
Special cases
When considering a few special cases, the concept of species become even harder to apply.
The Amazon molly (a fish) is a "species" that have "sexual intercourse" without having "sexual reproduction" and there are no males in the species! How is it possible? The females have to seek for sperm in a sister species in order to activate the development of the eggs but the genes of the father from the sister species are not used (Kokko et al. (2008)).
In an ant "species", males and females can both reproduce by parthenogenesis (some kind of cloning but with meiosis and cross-over) and don't need each other to reproduce. In this respect, males could actually be called females. But they still meet to reproduce together. The offsprings of a male and a female (via sexual reproduction) are sterile workers. So males and females are just like two sister species that reproduce sexually to create a sterile army to protect and feed them (Fournier et al. (2005)).
Bias
It often brings fame to discover a large new species. In consequence, scientists might tend to apply a definition of species that allow them to tell that their species is a new one. A typical example of such eventual bias concern dinosaurs where many new fossils are abusively called a new species while they sometimes are just the same species but at a different stage of development (according to this TED).
So why do we still use the concept of species?
Naming
IMO, its only usefulness is that it allows us to name lineages. And it is very important that we have the appropriate vocabulary to name different lineages even if this brings us to make a few mistakes and use some bad definitions.
The alternative use of the concept of lineage
It is important though that we are aware that the concept of species is poorly defined and that if we need to be accurate that we can talk in terms of lineages. The main issue with the term lineage is not semantic and comes about the fact that gene lineages may well differ considerably from what one would consider being the "species lineage" as defined by the "lineages of most sequences"... but this is a story for another time.
In consequence
In consequence to the above issues, we often call two lineages that can interbreed to some extent by different species names. On the other hand, two lineages that can hardly interbreed are sometimes called by the same species name but I would expect this case to be rarer (as discussed by @DarrelHoffman and @AMR in the comments).
Homo lineages
I hope it makes sense from the above that the question is really not related to the special case of the interbreeding between the Homo sapiens and the Homo neanderthalis lineages. The issue is a matter of the definition of species.
Video and podcast
SciShow made a video on the subject: What Makes a Species a Species?
For the French speakers, you will find an interesting (one hour long) podcast on the consequence of the false belief that the concept of species is an objective concept on conservation science at podcast.unil.ch > La biodiversité - plus qu'une simple question de conservation > Pierre-Henry Gouyon

Here is a related answer

The concept of species is imperfect in any definition.  But the oldest (and probably most function related definition) is that ability to cross breed to have viable offspring.  So under this definition, if the two populations can cross breed than they are not separate species.

Note also, that a few decades ago Neanderthal and "Cro Magnon" were considered to be part of the same species, homo sapiens. Cro Magnon would be Homo sapiens sapiens (subspecies) and Neanderthal would be Homo sapiens neanderthalis.  So under the traditional nomenclature, it would not even be so shocking to have seen some cross breeding!

Lately the fashion for species naming has departed some from the functional definition to other definitions.  In general ones that make species out of former subspecies. Sometimes this is for protecting certain creatures (legal issues of protection).  Often it is because academic biologists gain prestige from "discovering" species. (Very few of which lately are true in the field find a new animal discoveries, much more commonly being just nomenclature debates.)

[And don't get me started on mitochondrial DNA ("genetic proof") which many everyday people, like on Wikipedia, don't realize is not "the DNA" of chromosomes and of phenotypic recognition.  And for species with wandering males, the actual "genes" can be well mixed, but if the females don't travel much, you will see different mito DNA populations.]

*For example, look up issue of "ring species".


Can any enzyme be produced? After reading about how recombinant insulin is produced, the following question occured to me. Does the current level of technology allow any enzyme to be produced in a similar way?

As I see, producing amino acid sequences is not an issue. A possible difficulty I can think of is modifying the amino acid chains. In the case of insulin the problem has been solved. Are there some generally applicable solutions available to this problem, or do they have to be researched on a case-by-case basis?

Are there any other limitations to producing enzymes?

EDIT: As pointed out by P. Jay, the question might seem to suggests that insulin is an enzyme which it is not.

No, not all enzymes (or other proteins for that matter) can be obtained in functional form by recombinant expression with today's methods. As you suspect, problems arise when complex post-translational modifications are necessary to obtain the correct function.

Direct modifications to peptide is one potential problem. Some of these can be resolved by expression the recombinant protein in the right cell type: for example, expression in a bacteria may not provide the right modification, but expression in yeast or a mammalian cell might. CHO cells are a common mammalian cell type used in such cases; antibody production in hybridomas is another well-known example. But there are plenty of posttranslational modifications that are poorly understood, and most likely there are still many completely unknown types; new ones are still being discovered.

Another posttranslational event is association with cell membranes. Membrane proteins (including membrane-embedded enzymes, for example in lipid metabolism) can be very difficult to express properly, as not only the peptide but some surround membrane structure must be reproduced in the expression system to obtain correct function. This is also a major hurdle in obtaining structures for membrane proteins, notably many cell surface receptors. This article is a summary of the current challenges and unsolved problems in this area. And you can imagine the problems with proteins that need to form large superstructures to be functional --- large protein polymers, respiratory chain complexes, ribosomes, DNA replication forks ...

So there is no universal method; all proteins are different, some are easy to express, some are extremely hard.

Yes enzymes can be produced and even be optimized like restriction enzymes which are now mostly recombinant thou to low efficiency or biosafety level of source bacteria leaving that behind ,the greatest problem here is the size of protein and it's gene as when you produce artificial bio products you've got a prokaryote host to do that in cases which they do it out of cells then it's completely different but for sure possible the greatest problem is efficiency of production....and by the way insulin is not an enzyme


dNTP concentration for reverse transcription from RNA to cDNA Does it affect the results if I use the half of dNTP amount in a reaction that it says in my protocol?
I usually use 4 microlitres per reaction and this time I did a mistake and I used 2.

The final cDNA will be used for qPCR relative cuantification,so I am not sure if that will affect my results.

You will probably be fine. Lower dNTP levels might reduce the amount of product you obtained since it is usually the primers or the dNTPs that run out near the end of the reaction. The only other effect I am aware of is that the reaction might be slightly less specific as dNTPs sequester magnesium which is a big factor in determining the stringency of the reaction.

You say how many microliters you used but it would be more useful if you mentioned the concentrations of the dNTPs and the desired final concentration.


What is the name of this red plant? I came across this plant yesterday (14th May) and was wondering what it might be? Would anybody know the scientific name and if it's indigenous to the UK (personally I doubt it is)? The plant grows in an Asian style garden near Cumnock, Scotland.

Close up of leaves:

This is the "Acer palmatum" or Japanese maple, which shows a wide variety of different leaf forms (from here):

Specically you found "Acer palmatum dissectum 'Red Dragon'", for more information look here (picture also from this site):

Lace leaf maple you can also have a broad leaf. I have both zone 5 in Ohio


Pyruvate as a final electron acceptor in the electron transport chain During anaerobic respiration, why are electrons carried by NADH not transferred to the electron transport chain (ETC)? What happens is that lactate dehydrogenase reduces pyruvate to lactate, while removing H+ from NADH to form NAD+.

Why doesn’t pyruvate simply take the place of O2 as the final electron acceptor in the ETC during oxidative phosphorylation? Electrons would still be able to flow through the ETC and allow for the regeneration of NAD+, wouldn't they?

Someone else may come along later with a definitive answer but I found this question intriguing so here are my thoughts:

The standard redox potentials of the mitochondrial ETC carriers are:

NAD⁺/NADH              -0.32 V
complex I (Fe-S)       -0.27 V
complex II (cyt b₅₆₀)  -0.08 V
complex III ((cyt c₁)  +0.23 V
complex IV (cyt a₃)    +0.38 V
O₂/H₂O                 +0.82 V

Note that electron transport is carried out from negative to positive.

Now, for pyruvate/lactate the standard redox potential is -0.19 V so on the basis of this pyruvate could in theory accept electrons from complex I, but not any further down the chain. However, complex I normally transfers electrons to coenzyme Q within the membrane. The standard redox potential of CoQ is +0.04 V which is already too positive to be able to then reduce pyruvate at the membrane surface. Thus there would have to be a novel way of transferring electrons from the final FeS centre of complex I, which is within the membrane, to pyruvate. Pyruvate is, of course, soluble and is generated by cytoplasmic glycolysis, so this transfer would have be at the membrane surface that faces the intermembrane space of the mitochondria.

If such a scheme had evolved then it might be possible to achieve some proton pumping through the novel version of complex I, which would be  energetically advantageous.

Another complication is – assuming that a complex I with pyruvate as electron acceptor had evolved – how would the cell/ mitochondrion regulate electron flow during aerobic respiration? Presumably the pyruvate-accepting version of complex I would have to be kept inactive somehow until needed.

Clearly it is much simpler to have a soluble lactate dehydrogenase to deal with the pyruvate and regenerate NAD⁺.

Summary Answer

In anaerobic respiration the free energy change of the reoxidation of NADH by pyruvate is less than would be required to phosphorylate a molecule of ADP to ATP. The purpose of  the electron transport chain is to harness the much greater free energy change in the oxidation of NADH by molecular oxygen. So pyruvate can neither “take the place of O2 as the final electron acceptor”, nor would there be any point in modifying this complex machinery just so that it could be used by pyruvate to regenerate NAD+ when a single cytoplasmic enzyme (lactate dehydrogenase) will do the job.

More detailed numerical answer

This answer is taken from section 18.2 of Berg et al. and involves calculations of free energy changes from the redox potentials of the different half reactions and their relationship to the free energy of hydrolysis of ATP. It is worth careful reading, but I will summarize the key points.

Both pyruvate and oxygen can oxidize NADH, but the concomitant Standard Gibbs Free Energy change is very different in the two cases. This is the crux of the matter.
The standard redox potential for NADH → NAD+ is +0.32 V
The standard redox potential for Pyruvate → Lactate is –0.19 V
The standard redox potential for O2 →  H2O is +0.82

Combining these half-reaction redox potentials in the two oxidation reactions and then converting to standard free energy change (ΔG˚ʹ):

Oxidation of NADH by Pyruvate: ΔG˚ʹ = –6.0 kcal/mol
Oxidation of NADH by Oxygen: ΔG˚ʹ = –52.6 kcal/mol

But ΔG˚ʹ for ADP → ATP = –7.5 kcal/mol

So it can be seen that the energetics of the oxidation of NADH by pyruvate do not yield enough energy to synthesize even a molecule of ATP, never mind the approx. 3 that are obtained from oxygen. The electron transport chain is a device for breaking up this latter oxidation reaction into stages so that the free energy change can be used for generating the proton gradient that is used to generate ATP. It can only work with a powerful enough oxidizing agent.

The oxidation of NADH by pyruvate is useful, but only to regenerate NAD+ to allow glycolysis to continue and generate a smaller amount of ATP by substrate-level phosphorylation made possible by the glyceraldehyde 3-phosphate dehydrogenase reaction. For this oxidation only a simple enzyme, lactate dehydrogenase is required. There is certainly no reason to transport the pyruvate into the mitochondria (assuming they exist — think erythrocytes), which process, though incompletely understood, may well have an energetic cost.


Are all 23 chromosomes connected as one long strand of DNA? This has perpetually confused me. Is our genome made up of two long strands, each strand made up of 23 continuous chromosomes that bind together, or are they 23 free floating separate pair of chromosomes? I think it's the latter because I just learn that genes on different chromosomes assort independently, which would be hard if the genome was a long string, but I'm still not sure.

According to what I've learnt, we have 23 independent pairs of chromosomes. Each of them contains 2 chromosomes and different kinds of genes. The genes are connected in one strand. So it is the latter one. And the 23rd pair of chromosome is used to determine our gender actually. Females got XX and males got XY


Why exactly does the immune system weaken with age? Why does the immune system become weaker with age in humans and in some other mammals?  Let's try to be more specific than just "everything degrades with age."

We don't know.

More precisely, we know of many, many different reasons why the immune system deteriorates with age, but we don't really know which are different measures of the same thing, which are independent factors, which factors actually cause problems and which are harmless and incidental, and so on.

There are too many age-related phenomena to try to list. There's a nice recent review Aging and the immune system: An overview which spends time on

Aging and the immune cell repertoire
Cell Intrinsic defects in lymphocytes
"Inflammaging" ("an overall decrease in the ability to cope with different stressors, accompanied by a progressive increase in the organism's pro-inflammatory status")

Each of these broad topics can be broken down into dozens of sub-topics, and the molecular and evolutionary mechanisms underlying each are rarely well understood.

It's a huge area of research, and it's not possible to give a single concise answer.

Here is one known factor. A key component of the immune system is the skin and the protection provided by insensible perspiration, and the antimicrobial peptides in perspiration. However as humans perform less exercise with age, the proper habituation of the eccrine sweat ducts fails. The ducts normally balance the passing electrolytes, in particular conserving sodium chloride. The antimicrobials are only effective with the correct balance of electrolytes. If the balance is not correct, normal skin bacteria are able to enter the ducts and block them. With the ducts blocked the eccrine glands force sweat under pressure into the surrounding skin, destroying capillaries, and depriving the skin of oxygen. The protective live barrier is compromised and the skin becomes wrinkly. Extreme examples of the effect can be seen, particularly on the lower legs, in aged persons where the skin has a parchment type appearance.


Is the glomerular filtration rate, per kidney or for both? We say in a healthy human being the average glomerular filtration rate is about 120 mL/min. Is that for both kidneys together (60+60), or just one kidney?

Pardon me if this makes me sound like an idiot, because I have a feeling I'm thinking about this wrong.

The definition of GFR given in Wikipedia -

  Glomerular filtration rate (GFR) is the volume of fluid filtered from the renal (kidney) glomerular capillaries into the Bowman's capsule per unit time.

Since it is difficult to measure the volume entering into each Bowman's capsule, as a proxy, we measure the clearance of a solute that we know isn't going to be absorbed or secreted. For that particular solute,

GFR = (Urine concentration x Urine flow)/ Plasma concentration

The GFR you obtain here is the sum total of volume of all the fluid filtered from all the renal (kidney) glomerular capillaries into all of the Bowman's capsule per unit time.

Obviously, a single Bowman's capsule can't receive 120ml every minute, it is microscopic!!

So yes, the GFR or eGFR we use in clinical practice is the sum total of the function of both the kidneys. In fact, before transplantation, although the left kidney is preferred from the donor (since it is easier for surgery having a longer renal vein), it is more ethical to estimate individual GFR for each kidney and preserving the better functioning kidney. And yes, the total GFR drops after donating a kidney, but the body has sufficient reserve to manage.

If you still have a tough time figuring that out, think of them as many separate taps opened to fill a bucket. One tap for each glomerulus. The net rate of flow is the sum of flow rate in all the taps. The kidney has million such taps! And the taps are being clogged one at a time in chronic kidney disease - decreasing the GFR. And in a transplant, half the taps are suddenly shut down in the donor! But since this is a healthy kidney, the donor adapts and slowly reaches ~70% of original GFR.

It's a rate, not an absolute amount, so you wouldn't divide it up like that. It's like if a car is traveling 60 mph, each tire is going 60 mph, not 15.

You'd divide it up to describe the absolute amount, so if the kidneys filter 120 mL, then you could say each kidney filtered 60 mL (although even then each kidney isn't going to function identically).


How can the leakage of mitochondrial protons generate heat? I read the following about thermogenin:

  "When thermogenin is
  inserted into the inner mitochondrial membrane, it
  accentuates mitochondrial proton leak and dissipates
  the proton motive force. Since oxidation is no
  longer coupled to phosphorylation, thermogenin is
  said to cause uncoupling. In the presence of thermogenin,
  oxidation and proton pumping continue
  at high rates but with low rates of ATP synthesis. So Thermogenin enhances
  mitochondrial proton leak so there would be heat."

Why does proton pumping without ATP synthesis generate heat?

Uncoupling ATP synthesis from the ETC (electron transfer chain; this is where oxidation takes place) by thermogenin or any other method means that the energy used to generate or uphold the proton gradient gets 'lost'.

Since physics teaches us that energy is only transferred and never truly lost, the energy consumed by the ETC must most go somewhere - heat / thermal energy is the easiest and therefore most likely option.

References

Wikipedia article on Uncoupling Proteins
Uncoupling article written in chemical terms
Short general article about brown fat and heat production

Proton pumps just like any mechanochemical process generates heat, normally much of this heat is reclaimed in the production of ATP.  Without thermogenin proton pumps produce a proton gradient, the gradient is used to power atp synthase. thermogenin is a channel protein that creates holes in the membrane preventing a gradient from building up. The pumps never stops or slows so they continuously generate higher amounts of heat, which yields a higher temperature. It is basically the reason an electric motor running full throttle generates more heat than the same one barely running.

Basically brown adipose tissue evolved a way to generate heat by running a "motor" that is not attached to anything. Its not efficient but it is better than not having a way to consistently generate heat.

source 1

source 2

source 3

source 4


Why honey bees built hive in perfect hexagonal shape instead of irregular shape? Why honey bees built hive in perfect hexagonal shape ?

Due to Hexagonal shape, I can go near without any anxious or fear.( Apart from Honey bee's stings)

From this Question, Most creatures look like or tries to look like irregular to fear the other creatures to attack.

Why honey bees built hive in perfect hexagonal shape ?

Honeycomb cells (not the hive or the honeycomb itself) are hexagonal, in some species of bees but not all.  The regularity of this shape has puzzled people for a long time, and Darwin (and others before him) addressed the reasons for it.  Darwin did a series of experiments with bees, and summarized his results in Origin of Species.  You can search for "hexagon" in the linked text for his long explanation, or read the (still long) summary 'Evolution of Honeycomb on the Darwin Correspondence Project, but the short explanation is that it's the most efficient way to pack cells without wasting wax, and Darwin identified a bunch of intermediate (less efficient) cell structures in various bee species that supported his hypothetized mode of evolution.

  Thus, as I believe, the most wonderful of all known instincts, that of the hive-bee, can be explained by natural selection having taken advantage of numerous, successive, slight modifications of simpler instincts; natural selection having, by slow degrees, more and more perfectly led the bees to sweep equal spheres at a given distance from each other in a double layer, and to build up and excavate the wax along the planes of intersection. The bees, of course, no more knowing that they swept their spheres at one particular distance from each other, than they know what are the several angles of the hexagonal prisms and of the basal rhombic plates; the motive power of the process of natural selection having been the construction of cells of due strength and of the proper size and shape for the larvae, this being effected with the greatest possible economy of labour and wax; that individual swarm which thus made the best cells with least labour, and least waste of honey in the secretion of wax, having succeeded best, and having transmitted their newly-acquired economical instincts to new swarms, which in their turn will have had the best chance of succeeding in the struggle for existence.

in "the origin of species" pages 178 and 179, Darwin has stated that if a bee could build a cell slightly more hexagonal than the other bees then this bee would have a survival benefit since a perfect hexagon is the most economical structure in storing the greatest amount of honey with the least amount of wax, but unfortunately there is nothing in his analysis that proves the point. He concludes on page 179 that the saving of wax by largely saving honey would be an important element in the success in any family of bees.
The problem with that analysis is that a slight modification of structure in this case a slightly more regular hexagon cannot provide a survival benefit as the two structures are almost identical.(the old cell and the slightly modified cell)


Are Triceratops and Eotriceratops similar enough to be considered as the same genus? Everybody knows Triceratops, the horned dinosaur from Late Cretaceous North America, who lived 68-66 MYA.

In 2007, Eotriceratops xerinsularis was named and described (Wikipedia). It lived in (what is now) Canada about 68 MYA. It is a little bigger than Triceratops but in many aspect very similar, e.g. they both have long horns and solid frill, and postcranial skeleton. Gregory S. Paul, in his Princton Field Guide to Dinosaurs 2016, suggested putting Eotriceratops xerinsularis in the same genus as Triceratops, renaming it to Triceratops xerinsularis. I find this suggestion appealing, but I know Paul's taxonomy is unorthodox and not mainstream (e.g. I do not agree with the thesis that Torosaurus is merely a full adult Triceratops).

So the question is: can Eotriceratops xerinsularis be put in the same genus as Triceratops and is this suggestion is plausiable enough?

Taxonomists have wide leeway over assigning higher taxa. The publication process in which Eotriceratops was described as a new genus made it a new genus. However, given a different set of reviewers, they may have rejected the new generic description, and suggested that the author put it into Triceratops. The process is somewhat arbitrary, and there are some random elements to higher taxon assignment. But it is the system we use. If somebody were to write a paper to synonomize Eotriceratops with Triceratops, and that paper were accepted, then Eotriceratops would cease to be a valid name. Its all about publication precedence. Gregory  Paul may have good reason for his suggestion, but it must be published before a change is made.

Eotriceratops was a larger species of triceratops so they both were similar in name but different in size
Well eotriceratops was a larger ceratopsid but both of them had different predators for example the triceratops horridus was hunted by the T-Rex but for the eotriceratops I don't what predators it had


Does bleach destroy RNAse activity, and if so, how does it do it? I am working with RNA samples, and I'm trying to be very careful about RNAse contamination.

I have some questions about bleach, though. Some people say that a solution of bleach is enough to destroy RNAse activity, but is it really? How does it do it?

I'm not sure if wiping the surface using a solution of bleach would be enough to kill RNAse activity, or if it is necessary to use products such as RNAseZap or RNAseAway.

RNAses are enzymes, and there are various ways to inactivate them. Unfortunately, RNAses are rather stable proteins and autoclaving doesn't completely kill their activity. The common methods to inactivate are unspecific methods that will destroy any enzymes, either through covalent modification or degradation.

The most common methods for RNAse inactivation are:

Treatment with DEPC. This covalently modifies histidine and a few other amino acids, which will inactivate RNAses.
Heating to 200-250 °C for at least an hour, this is most commonly used for metal and glass equipment
Incubation with 1M NaOH for an hour at 37 °C, which will hydrolyze proteins

Using bleach is not a method I've used, but it should work in principle as hypochlorite will react with proteins.

I think they are asking how to clean surfaces like benchtops.

Bleach might work. But a better solution would be to get a box of aluminum foil. The processes for making the foil are very harsh, so it's doubtful any protein would survive the process, not to mention that there are no proteins involved in aluminum manufacture to contaminate the process. Just be sure to always use gloves when handling the foil or you'll contaminate it.


What is the term for awareness of or inclusion of real sounds within a dream? I fell asleep while listening to a podcast, and I am sure I was dreaming but I could also still hear the podcast.

The podcast played an important role in the dream, I was searching for the source of the voice, wondering if others in the dream could hear the same voice. I started to feel a bit panicky and woke up as the podcast also happened to end. I rewound the show and confirmed that it was all there, exactly as I had heard in my dream!

I would like to read more about this type of experience, but I am having trouble finding the right words to search. Is there a name for this phenomenon? Is there anything that contributes to experiences like these? I know it wasn't lucid dreaming, because I wasn't aware of being asleep.

I think I found a good expression : "sensory incorporation in dreams"

https://www.psychologytoday.com/blog/dream-factory/201409/sensory-incorporation-in-dreams

It doesn't seem reflected in a Google Scholar search however, and I don't find a consistent terminology in the papers that do seem to be about the subject. That article can be a good starting point though.

EDIT: other good one: "influence of external stimuli on dreams".

https://journals.ub.uni-heidelberg.de/index.php/IJoDR/article/view/15754

My answer is going to be verily based on my experience and thinking, so don't take it for absolute.

When we are dreaming, at the level of the brain, sensual (meaning from senses) experience is being created by projection in the sensitive cortices (visual, auditive, somatic...) from other zones of the brain. In this way the brain is creating a sensitive environment and experience to the self, which, usually unaware that it is a dream, lives through it, making decisions, solving problems, having experiences, remembering and even learning.

In your case, it seems that, while you were dreaming (creating a sensory experience from the "inside"), you were also being sensually stimulated (meaning form the "outside", through a real sensitive organ - the ear). The input from your audition, though not enough to wake you up, still originated the corresponding projections in your auditive cortex, creating the matching experience of hearing the podcast and overlapping it with the experience that was being generated in the dream. This way, the sound of the podcast was incorporated in the experience created in the dream, affecting it in the process.

I tried to explain this in the most biological (neurological) way I could!


Can a bacterium express a virulence gene and not produce toxins and what may be the cause of this? I am preparing a seminar on viable but non-culturable (VBNC) state in bacteria, mainly foodborne pathogens and I just saw this line in a journal article by Lothigius et al that "the expression of the virulence gene in VBNC cells does not necessarily indicate the cells will produce toxins". Any explanation on what this statement means?

Lothigius, Å., Sjöling, Å., Svennerholm, A.-M., & Bölin, I. (2010). Survival and gene expression of enterotoxigenicEscherichia coliduring long-term incubation in sea water and freshwater. Journal of Applied Microbiology, 108(4), 1441–1449.

To expand a bit on @Mohamed's answer, there are several mechanisms by which virulence gene products can be up- or down-regulated without changes to mRNA expression.
Post-translational modifications
Adenylate cyclase-hemolysin (AC-Hly) is a toxin produced by the Bordetella pertussis, the causal agent of whooping cough.  There are very few amino acid differences between the AC-Hly of B. pertussis and closely related Bordetella species.  Palmitoylations of lysine residues on the C-terminus of the B. pertussis AC-Hly are necessary for its specific cytotoxic activity.  [Bouchez 2017]
RNA secondary structures
After transcription, mRNAs can form secondary structures by base pairing, preventing ribosome binding and translation.  For some pathogens, virulence gene mRNAs forms these structures, which melt at human body temperature, allowing for fast production of toxins without the need to increase virulence gene transcription. [Narberhaus 2010]

Gene expression means making mRNA and then translated to protein. Their might be many steps unders regulation in this path where a gene makes mRNA but then that mRNA is not translated (like degraded or inactivated).


Immune response to shock I am studying nursing and have a question regarding the physiological response to shock (decreased perfusion).  In lecture notes supplied by the lecturer, he indicates that there is a neural, hormonal and immune response to shock that is compensatory.

The neural component is the activation of the sympathetic nervous system, and hormonal response is through RAAS, etc.  This makes sense, as these mechanisms attempt to increase blood pressure and blood volume

I don't understand the immune response, though, which is described as the release of pro-inflammatory mediators, which lead to endothelial cell damage, making the vessels leaky, leading to oedema.  So how is the compensatory, it seems disruptive?  And why exactly would pro-inflammatory mediators be released in response to shock in the first place?

First: what is inflammation.  From wikipedia
https://en.wikipedia.org/wiki/Inflammation

  Acute inflammation is the initial response of the body to harmful
  stimuli and is achieved by the increased movement of plasma and
  leukocytes (especially granulocytes) from the blood into the injured
  tissues. A series of biochemical events propagates and matures the
  inflammatory response, involving the local vascular system, the immune
  system, and various cells within the injured tissue.

Second re shock: why does it happen?  If I go into shock from blood loss after a terrible knife juggling accident I will probably not have the inflammatory piece: I am dying from lack of blood and consequent low blood pressure.

What if I am in septic shock?  That means shock caused by organisms, usually bacteria, in the blood stream.  Bacteria are the ancient enemy and we have layers upon layer of defense accumulated over evolutionary time.  The reason we have them is that somehow, our ancestors that had them had some fitness advantage - probably because they survived having bacteria in the blood.

Some of the stuff that comes with that package does not seem very adaptive - like the leaky vessels and lungs filling up with fluid.  Maybe we see the wild extreme of this reaction but to a lesser degree (lesser infections?) those inflammatory responses are good?  Maybe releasing a storm of neutrophils has unavoidable side effects for the surroundings - like the Avengers fighting an alien army in NYC?  It was tough on NYC.  Maybe those extreme shock reactions save the organism 1 time in 10, which is better than the odds otherwise with an overwhelming bacterial infection.

Bottom line though is that bacteria in the blood in great numbers is an existential threat to the organism.  Desperate times call for desperate measures.