What evidence gives clues to the physiological basis for conversion disorder?

It's usually important to rule out other medical conditions when considering many psychiatric diagnoses due to similarities in symptoms between them. There are many examples but I'm not sure if it's appropriate to note them here as a lot of symptoms have to be considered in a clinical context and might be mistaken as medical advice. It's also important to note that concurrent medical and psychiatric conditions frequently occur with individuals diagnosed with conversion disorder.(2).

Conversion disorder was previously combined with somatisation disorder and was known as hysteria.(2). Conversion disorder is a diagnosis of exclusion where the symptoms are not a result of:

neurological or other medical condition;
the effect of a substance; or
cultural behavior or experience.(1).

The key is that these are not intentionally or medically driven symptoms but rather physical manifestations of psychological needs ("unconscious manifestations of emotional conflict"(3)). Psychoanalytic theory suggests that "conversion disorder is caused by repression of unconscious intrapsychic conflict and conversion of anxiety into a physical symptom"(2).

In terms of physiological basis of conversion disorder, it's been suggested that an imbalance in metabolism between the dominant and non-dominant brain hemispheres; and impaired communication between the two may be an issue.(2). There are some other points you can also read at MedScape.

Ferri. Ferri's Clinical Advisor. 2012. Mosby.
Sadock. Kaplan & Sadock's Synopsis of Psychiatry. 10th ed. 2007. Wolters Kluwer.
Jacobson. Psychiatric Secrets. 2nd ed. 2001. Hanley and Belfus.


This is a pretty broad question, but I will try to give an answer:

This process will undergo further evolution over time, no question. It has evolved into the current state and there is no reason to assume that this ended. When there are mutations which prove advantageous, they will evolve. This may also involve a faster response time for example, but we can of course make not definite claims about it.

There are antigens which are not recognized by the immune system, the process is called molecular mimicry. In it, microorganisms mimic molecules or structures which are found inside the body of the infected person and which are therefore not recognized by the immune system (if the immune system recognized self-antigens, this leads to autoimmune diseases). Have a look at the references 1 and 2 for more details.

This is a rather theoretical question. Our immune system is really efficient in clearing potential threats before you get a real infection. You can see the difference when you compare healthy individuals with persons which are immuno suppressed because of a transplantation. These persons need to be very careful about their environment in avoiding the exposure to potential pathogens. And they easily get infections. Additionally microbes evolve to evade our immune system. So I think the answer here is no.

These are viruses which co-evolved with the organism, an example would be the ebola virus in certain fruit bats. Here it does no harm, while it is a big problem for humans. As there is a really, really big number of viruses available in nature, it is quite unlikely that we learn to tolerate all of them. Additionally viruses mutate and change over time, so we would have to learn again to live with them.

References:

Molecular mimicry
Molecular mimicry and immune-mediated diseases.


Are there any exceptional cases in which a person with O negative blood group cannot donate?

There are some situations, where, depending on the interpretation of Rh status, an exception could become possible. Rh +/- commonly refers to the D antigen. However, the Rh group has many antigens in it, including C and E. One can become sensitized to these other antigens and develop a hemolytic response to incompatible C or E type.

Dean L. Blood Groups and Red Cell Antigens [Internet]. Bethesda (MD): National Center for Biotechnology Information (US); 2005. Chapter 7, The Rh blood group.


How to store vegetables in the refrigerator: In plastic bags or not?

Based on what I've been able to locate on the USDA website:
Refrigeration & Food Safety

It would be better to take the foods out of the bags and put them in the crisper if you're using the crisper solely for vegetables:

  Some refrigerators have special features such as adjustable shelves, door bins, crispers, and meat/cheese drawers. These features are designed to make storage of foods more convenient and to provide an optimal storage environment for fruits, vegetables, meats, poultry, and cheese.

And:

  Sealed crisper drawers provide an optimal storage environment for fruits and vegetables. Vegetables require higher humidity conditions while fruits require lower humidity conditions. Some crispers are equipped with controls to allow the consumer to customize each drawer’s humidity level.

Therefore, keeping your stuff in the bag would negate the purpose of these specialized compartments. Too bad the USDA doesn't specifically address the issue of bags...


This is actually far more complex a question than you probably know. The country you are writing from matters. There are some rabies virus variants that have a relatively low pathogenicity for humans (dog rabies is one of these; a relatively large innoculum is required, i.e. a bite, commonly a deep one with lots of virus-laden saliva.) The likelihood of canine-associated rabies developing from a non-bite exposure is extremely low; in fact, the exact risk is unknown.
In the US, enzootic (dog-to-dog) canine rabies virus has been virtually eliminated through vaccination and stray control programs, making wild animals (including feral cats) the primary concern. Depending on the country your friend lives in, dogs may not even be high on the list of worrisome sources.
Regarding canine-associated rabies,

Rabies control was accomplished [through dog vaccination programs, responsible pet ownership, and serious population control of stray dogs] in Europe, North America, Australia, Japan, Taiwan, Malaysia, and Singapore.

If you don't live in one of these countries/continents, dog-associated rabies is still a major concern. If you do live in the mentioned areas, you can probably dip your hand in dog saliva and not be concerned.
Rabies is usually contracted by a bite; that is most common.

The most dangerous and common route of rabies exposure is from the bite of a rabid mammal. An exposure to rabies also might occur when the virus, from saliva or other potentially infectious material (e.g., neural tissue), is introduced into fresh, open cuts in skin or onto mucous membranes (nonbite exposure). ...Exposures to bats deserve special assessment because bats can pose a greater risk for infecting humans under certain circumstances that might be considered inconsequential from a human perspective.
how exactly does the process of infection happen, and how can it happen?

The exact way it happens is not completely understood, but that answer won't help you convince your friend of anything. The virus is usually deposited in tissue near a cutaneous (peripheral) nerve. If it gains entry to the nerve, it makes its way to the brain with the typical disastrous results.
Having said all this, your friend is not going to stop worrying, because the virus is only the focus of an irrational fear. Though the foci of irrational fears are fairly stable, OCD is most likely the underlying problem, and conventional rational discourse doesn't really suffice in curing the obsession.
During 1990-2007, 34 bat-associated human cases of rabies were reported in the US: 6 cases reported a bat bite; 2 cases reported a probable bite; in 15 cases, physical contact was reported (e.g., the removal of a bat from the home or workplace or the presence of a bat in the room where the person had been sleeping), but no bite was documented; and in 11 cases, no bat encounter was reported, but the rabies virus was bat-specific.
Any encounter with a bat, even a dead one (as stated above), must be evaluated for possible post-exposure prophylaxis.
Unfortunately, in the US, animal rabies is common, and at least 23,000 persons/ year receive rabies postexposure prophylaxis (PEP). (It is probably considerably higher, as no reporting mandate exists.) With the elimination of canine rabies virus variants and enzootic transmission among dogs, human rabies is now rare in the United States, with an average of one or two cases occurring annually since 1960.
In the US in 2013, of the three human cases reported, 2 were involved in organ transplants (raccoon rabies virus variant) and one was a Guatemalan (canine rabies virus variant).
In 2012, one human died from an exposure to a bat. He touched a bat under a bridge. He did not report a bite to a witness. He became ill while traveling, and died in Switzerland. A number of humans exposed to his saliva (including his Swiss caregivers) received PEP.
*Some people in high-rabies areas without the illness have been documented to have developed antibodies to rabies. The mechanism is unknown.
Human Rabies Prevention - United States, 2008
Pathogenesis of Rabies
A Single Amino Acid Change in Rabies Virus Glycoprotein Increases Virus Spread and Enhances Virus Pathogenicity
Human Rabies Prevention (Comment From a Canine‐Rabies‐Endemic Region)
Epidemiology of rabies post-exposure prophylaxis—United States of America, 2006–2008
Rabies surveillance in the United States during 2013
Use of a Reduced (4-Dose) Vaccine Schedule for Postexposure Prophylaxis to Prevent Human Rabies: Recommendations of the Advisory Committee on Immunization Practices


How is a T lymphocyte specific to an antigen but not specific to an epitope?

For this answer lets restrict ourselves to T dependent MHC II mediated responses.

So, an APC like a macrophage or a dendritic cell, takes in a pathogen by phagocytosis and degrades it inside the cell. Some of its broken proteins, which are antigens are presented on the MHC II of this particular APC.

The B cells also do something similar but they identify either free floating antigens or the ones that are expressed by phagocytic APCs. These antigens are broken down in the lysosome. These fragments now are expressed on the surface along with MHC II. This fragment may or may not contain the epitope that the B cell receptor (surface antibody) originally recognised the antigen with. Also, it is not that just one of the fragment is taken to the surface, most of them make it, each with a separate MHC.

The T cell that is going to now interact with this B cell may have a TCR (T cell Receptor) against the epitope in any one of those fragmented antigens on the MHC.

This T-cell is specific to that particular epitope of the antigen it bound to, similarly there could be another T-cell that could recognise some other fragment of the same antigen brought to the membrane by a different MHC II.

So, the epitope that the B-cell and the T-cell recognised the antigen with, needn't be the same. But logically, there's a possibility that they may be.

Note that:

The processing of antigen in the phagocytic APC is not shown in the picture.
B cell recognises antigens not that are displayed on the MHC II (this the T cell does) but those that are tethered on the APC membrane.

Image: Nature Reviews Immunology.


Why do we have wrinkly fingers after swimming?

Great question, for which still no definite answer is known despite ~100 years of research.

A simple physical basis for the wrinkling however seems unlikely as glabrous skin without sweat glands does not wrinkle, and as wrinkling requires the activity of specific nerves.

Moreover plausible evolutionary ideas, which used to be popular, such an anticipated improved ability to grab, don't appear that clear in newer experiments.

For the information above, and an even more detailed answer, please see Haseleu, Omerbasic et al. 2014 http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0084949


From a certain point of view you could argue that our bodies have an inherently limited lifespan;

Telomeres are extensions to the end of chromosomes that prevent damage or loss of genetic information during cell division. Telomeres are not replaced (in normal cells), which gives rise to a replicative lifespan; the number of times a cell can divide before permenantly leaving the cell cycle (senescence).

This is generally viewed as an anti-cancer mechanism to protect against errors creeping in to the genome through many cell divisions. In order to become cancerous, a cell must first overcome its replicative lifespan [ref.]. This is achieved by activating the (normally inactive) telomerase enzyme that extends the telomeres - embryonic stem cells are one of the few cell types that normally express this enzyme.

There are other ways in which you could argue that our lifespans are fundamentally limited, but it is important to note that the objective is not 'to die', but to increase fitness (in a Darwinian sense) earlier in life. This is known as antagonistic pleiotropy; when an advantageous trait early in life is disadvantageous later in life.

Telomere shortening is just one example of antagonistic pleiotropy (protects against cancer when younger, but limits the number of times your cells can divide).

Other traits that inherently limit lifespan include;

Neurons (as a rule) do not replicate, and last for your whole life time. This certainly excludes them from replicate senescence, however it means they are highly susceptible to 'wear and tear'; oxidative stress is a natural by-product of respiration, and the vast majority of damage done by these species (e.g. reactive oxygen species) is repaired by the cell, however some will always remain unchecked, and eventually this leads to neurological dysfunction and cognitive decline. Without intervention this is inevitable in each individual (the rate of aging differs between people, but aging and age-dependent diseases are disorders are a natural part of living).
The same is true for cardiac and smooth muscle - whilst much repair can be carried out, it is inevitable that damage will creep in over a life time, and thus the vast majority of human age-related deaths are due to cardiac problems in one way or another.

So there is no 'programmed' limit to life span, in that we have not evolved to die, but our bodies are inherently limited by the systems that have evolved. Life expectancy a few thousand years ago was ~20 years (if you lived beyond infancy!), whereas now in the developed world this is ~80 years, so our bodies can already survive way beyond our 'natural' life span, and thus we now succumb to age-related disease. Evolution has spent millions of years giving us every possible advantage that leads to reproductive success. Natural selection of traits beyond reproduction are secondary to those beforehand, and thus we have fundamentally limited life spans.

There is an argument for an evolutionary advantage of limited lifespan. This seems at first counter-intuitive, until you consider that natural selection does not act on individuals, but genes. It is proposed to be advantageous (in some circumstances) for an organism to have a shorter life span, as this increases the turn-over of individuals in that population. This in turn increases their evolvability - clearly advantageous for the gene(s) influencing this trait if it increases the likelihood of successful reproduction and thus passing on that gene/allele/trait...

I like this hypothesis, and can see that natural selection may favour it. I think mice are great examples here; they have much shorter lifespans than us, yet they 'age' (biologically) the same (cardiac problems, diabetes, cancer) but at a faster rate to give a higher population turnover). In a high mortality environment, the most adaptable animals will be more successful.

However, I think this is likely to be secondary to the pressures on other survival traits that  more directly increase the chances of successful reproduction.


How can I obtain a computer readable model of Dr. Gerhard Michal's biological pathways map?

Roche's Biochemical Pathways works as a big png image and just put labels on the map. But you could try to extract data using queries like http://biochemical-pathways.com/pol/fts/query?query=Glutarate
It seems to be legal as it's not prohibited.

Escher is a good pathway visualization tool where you can save map in JSON or SVG.

Another choice is VMH (Virtual Metabolic Human) - the virtual metabolic human database provides literature-derived information on human metabolism, gut microbial metabolism, nutrition, and diseases.

Reactome has two layer map - first layer is biological interactions, second layer is pathways.


What is the name of this injured species?

Well, after a lot of research, I hardy believe that it is a Rhizotrogus aestivus. First of all, the size (2-3cm) you mentioned fits exactly. Secondly, the colour matches fair enough. Finally the antennas and the body shape, may not be seen very well in the picture but I assume that they match. The only thing that I am not sure is the "laziness" of that insect, beacause they are only lazy or clumsy and not active, only when they are about to die.

For more informations check here: https://inpn.mnhn.fr/espece/cd_nom/10907?lg=en


Comparative evolutionary study: is amino acid or nucleotide comparison more useful?

Each has its own utility, depending on the time-frame you are looking at. For evolutionary studies, you need variation, but not so much variation that one substitution at the same position overwrites a previous substitution. So if you are looking at deep splits, over hundreds of millions of years, it may be that amino acids are more reliable. But you are correct in that since they are functionally more important than silent substitutions (nucleotide changes that don't change the amino acid), it is possible to have amino acids converge on the same state, independently. Nucleotides do this too. Both require statistical models (maximum likelihood) that accommodate the possibility of multiple changes at the same site. If you are looking at recent evolutionary splits, there may not be enough (or any) amino acid changes to compare, so in this case, nucleotides would be better. You would not measure continental drift with a stopwatch, or a 100-meter dash with radiometric dating.


Ribosomes don't read DNA.
Transcription adds several layers of regulation tactics: you can control transcription itself, you can control mRNA.
mRNA amplifies genetic information that you need at the moment. Having many copies of a matrix really helps.
Some prokaryotes have splicing. It's not a good idea to splice your DNA.

EDIT per your request of some elaboration.

  Why did they evolve to read RNA in the first place as they are primal
  to all other organisms, why did they develop this

The "RNA world" hypothesis (which is the most realistic early life model, considering the ever-growing body of evidence) postulates that RNA had been the main thing long before DNA was introduced into cells. The ribosome (being an RNA enzyme that doesn't require any proteins to bind amino acids together), along with many other RNA enzymes and regulators, is believed to be a relic of that world. Wiki has a good page with all the references you might want to read.

  Also, the regulation tactics, isn't DNA free floating and so are all
  the replication enzymes like Helicase, primase and RNA primer etc. So
  how do they regulate the action of these enzymes as they are just free
  floating?

First of all, it's a common misconception that prokaryotic cells are mere bags stuffed with enzymes and whatever. Prokaryotes posses highly complicated compartmentalisation systems (some even possess nucleus-like compartments). Second of all, DNA is not "free floating": it's located at a specific site with a special molecular environment. If you want details, ask a separate question, or better a series of questions with narrow scope, because bacterial regulation is too diverse, bizarre and sophisticated to cover here (we had a 3 years-long course on this matter when I was a student).

  Could you explain a bit of how the extra copy helps as is it not just
  more data to deal with?

When you have many copies of a matrix, many ribosomes can synthesise a protein at once. This comes in handy when you need to make tons of something as fast as possible. Remember, ribosomes are quite ubiquitous in all active cells for this very reason: to facilitate fast protein synthesis (at least as far as copiotrophic organisms are concerned).

  What exactly do you mean by splicing?

I mean splicing: a group of processes by which introns are excised from primary transcription products.


Do bacteria exist which live exclusively on non-organic matter?

Sulfate reducing bacteria get their energy converting sulfate to hydrogen sulfide. They are relatively common and may have been the source to turn some oil/gas deposits "sour". Specifics in Wikipedia.


For grasses leaves tend to be inedible due do with the high quantity of silica deposited in the leaves to form structures known as phytoliths Wikipedia.

While this has been shown to inhibit digestion by insects (Hunt et. al., 2008, Massey et.al., 2006), I'm not aware of any studies on how this affects digestibility for humans.  There are however anecdotes about people starving to death with grass stains around their mouths during the Irish Potato famine.


Concentration of caffeine in physiologically relevant setting

Let's figure it out. Suppose an adult with an average blood volume of 5 L (5000 mL) drinks a cup of strong coffee with 100 mg of caffeine in it. Given caffeine's formula weight of 194.19 g/mol, and assuming 100% of the caffeine is in the blood stream, its concentration (from this awesome calculator page from Graphpad, the makers of Prism) would be approximately 103 µM, or 10-40 times less than what's being used in the experiments you cite.

Of course, this is overcoming drug-mediated cell cycle arrest, so its possible that a lower concentration is needed to jump-start physiologically-arrested cells.


Cell cycle

Talking about physical copies of gene, we would indeed have at least 1 copy during the haploid phase, 2 copies during the diploid phase and 4 copies during the mitosis (and during the first phase of the meiosis). Of course, species having mitosis during the haploid phase would have 2 copies of the gene during the mitosis. I am not talking about polyploid species and am not talking about some fungi and other things that have all kind of crazy reproductions system. I am not talking about mtDNA either. Finally, I am not addressing the case of specialized cells that lose part of their genome or the case of tissues that are basically cells who merged together, so that the concept of cell does not even hold any more such as the Syncytiotrophoblast (in the placenta) (see also cell fusion and syncytium).

In short, the variation in the number of copies during the life-cycle is very dependent on the species of interest, the sequence of interest and may also fall under some semantic issue about what is a cell. Note another potential semantic issue result from the question "how similar two genes have to be to still be called copies?".

Mutations and polymorphism

Now, some genes can be found in several copies. When, in a given population the number of copies of a given gene varies from one individual to another, we talk about Copy-Number Variation (CNV). The increase in the number of copies is called gene duplication (or gene amplification or chromosomal duplication when a very big chunk of DNA gets duplicated). The decrease in the number of copies is called gene deletion. There are a diversity of processes that can cause deletions and duplications such as homologous recombination, retrotransposition event, aneuploidy, polyploidy, and replication slippage.

Evolution of CNV

What mutation is likely to occur first

Gene duplication does not necessarily yield to an increase in the protein concentration (but it can as it is the case for the Pelizaeus–Merzbacher disease for example). If higher expression is selected for, it "feels more likely to me" that the first mutation(s) allowing for this increased expression will affect the regulatory sequences and will not increase the number of gene copies.

Consequences of gene duplications

Gene duplication (if not loss) can yield to subfunctionalization or neofunctionalization. From wikipedia:

  Subfunctionalization [is a process] in which pairs of genes that originate from duplication, or paralogs, take on separate functions

...In others words, copies are free to accumulate mutations as long as the other copy is still doing its job

  Neofunctionalization, one of the possible outcomes of functional divergence, occurs when one gene copy, or paralog, takes on a totally new function after a gene duplication event

...Basically, one copy gets a totally new function... that can yield to very interesting innovations such as anti-freeze proteins (ref) or snake venom (ref).


This is my take in this, without experience of using the Taylor series to analyse evolutionary game theory problems.

As you know the Taylor series expansion of $f(x)$ at point $a$ can be written as:

$f(x)= f'(a)(x-a) + \frac{f''(a)}{2!}(x-a)^2 + \frac{f^{(3)}(a)}{3!}(x-a)^3 + ... + \frac{f^{(n)}(a)}{n!}(x-a)^n + ...$

Often factors above second order are dropped as a simplification. However, to use the Taylor expansion, the function must be differentiable at point $a$, and to be differentiable it must be continuous.

As @Artem Kaznatcheev writes in his question, "...with weak selection meaning the game modifies overall fitness only slightly..." and "... it is typical to model organisms as having a base fitness that is modified slightly by the game interaction...". These statements imply that the overall fitness function/surface can be assumed to be relatively smooth and continuous (i.e. the payoff is negligible), which means that the Taylor series expansion can be used. If the game payoffs for a single game would determine a large proportion of the overall fitness, the fitness surface would be discontinuous.

An example where a Taylor series expansion is used to simplify the fitness function under weak selection is given in Andre & Godelle (2006) (see equation 20 ff).

You might also find this supplement to Nowak et al (2010) interesting (a rather controversial paper), especially page 8.


Why does vitamin D need to be exogenous?

Vitamin D is vitally important for the uptake of calcium, iron, magnesium, phosphate, and zinc, as well as for bone maintenance:

  Vitamin D promotes calcium absorption in the gut and maintains adequate serum calcium and phosphate concentrations to enable normal mineralization of bone and to prevent hypocalcemic tetany. It is also needed for bone growth and bone remodeling by osteoblasts and osteoclasts. Without sufficient vitamin D, bones can become thin, brittle, or misshapen. Vitamin D sufficiency prevents rickets in children and osteomalacia in adults. Together with calcium, vitamin D also helps protect older adults from osteoporosis.

It also acts as a hormone, binding to the Vitamin D receptor in the nucleus of target cells which then acts as a transcription factor for genes related to multiple processes:

  Vitamin D has other roles in the body, including modulation of cell growth, neuromuscular and immune function, and reduction of inflammation [1,3,4]. Many genes encoding proteins that regulate cell proliferation, differentiation, and apoptosis are modulated in part by vitamin D. Many cells have vitamin D receptors, and some convert 25(OH)D [an inactive form] to 1,25(OH)2D [an active form].

So, the truth is far from your statement that "Vitamin D doesn't really do anything chemistry-bound, but rather just works as a hormone matching some arbitrary protein receptors or something." In fact, a cursory reading of the first couple of Google results for "Vitamin D" shows that it is broadly involved across the body in many different processes ranging from inflammation and cancer to bone maintenance and mineral absorption.

Sources:

Vitamin D - Fact Sheet for Health Professionals. NIH Office of Dietary Supplements. November 2014.
Vitamin D Wikipedia
Effectiveness and safety of vitamin D in relation to bone health. A Cranney, T Horsley, S O'Donnell, et al. Evid Rep Technol Assess (Full Rep). 2007 Aug;(158):1-235.
Vitamin D WebMD


In an evolution mutations are often random and lead to differences in phenotype that can be adaptive under certain pressures.  A lot of times mutation is a random process, but here are three cases I can think of off of the top of my head where I would say the organism is 'trying' to do it:

HIV is a retrovirus, which means in its viral form its genome is single stranded RNA, which is then converted into double stranded DNA within the host.  That conversion is carried out by a virally encoded reverse transcriptase.  This enzyme has a much higher error rate when making the RNA into DNA because it cannot proofread like our DNA polymerases.  This means that HIV mutates incredibly fast.  Many of these mutants are not very fit, but since there is so much selective pressure against staying the same due to attack from the immune system, some mutants will be much more fit if they can avoid that attack.  Its a numbers game, and by making lots of random mutants HIV is very good at it.

A related, but different case is found in the diversity generating retroelements of certain bacteriophages.  These are double stranded DNA viruses that infect bacteria.  The bacteria these viruses infect could mutate to escape the viruses by losing a certain receptor that the virus binds to.  It was observed however that the the virus would mutate incredibly quickly to bind to a different receptor, a lot faster than would be expected for a DNA virus.  Also, it was found that these viruses contained reverse transcriptases, which is bizarre, since there is no reverse transcription step in a dsDNA viral life-cycle (so we thought).  To make a long story short, this virus will transcribe the DNA that codes for its binding proteins into RNA, then use its reverse transcriptase to turn that RNA BACK into DNA, but uses a sophisticated targeting strategy so that it only mutates the region that is used for binding to the bacteria.  It will only mutate adenine residues, leaving the C's, T's and G's alone.  This is a much more clever system than HIV, because this virus uses site-specific mutations on its binding feet, and doesn't mutate its core proteins, the mutation of which would probably just lead to viruses that couldnt replicate.  Here a reference for the interested: http://www.nature.com/nature/journal/v431/n7007/abs/nature02833.html

Just so you dont think this is reserved to viruses, we do this as well with our immune system.  In order to recognize antigens in attacking pathogens, our immune cells have two methods for making diverse, random, receptors.  First is V(D)J recombination, where the multiple diverse copies of the V, D and J regions of antibodies and receptors are combined at random to make one set.  Wiki says theres 3x10^11 possible combinations here.  After that, theres also somatic hypermutation during the proliferation of B cells.  In this process, the random mutation rate is hugely increased in the region of the B cell receptor gene, specifically for making slightly different versions of the already 'OK' receptor to make it a great receptor.

General theme: raising your mutation rate, either across the board(HIV) or specifically (DGRE and SHM) is a good way to intentionally add randomness for a beneficial purpose (to the extent that you can attribute 'intent' to a viral particle).


Subtracting shared DNA with half-sibling

The website is just wrong when it says for DNA tests on a person and their half-sibling:

  In other words, you and your half-brother should be able to figure out what part of your DNA came from your mom.  And if you subtract out that shared DNA, what is left must have come from your dad!

Consumer autosomal DNA tests do not identify which of the two chromosomes present in the sample a detected variant can be assigned to.  The tests show only the two variant values detected at each location tested, and not which chromosome they come from.

Using this data from two tests, comparisons can show stretches of chromosomes which have matching patterns of variants which indicate with good probability that the corresponding pieces of chromosome have the same origin.  The tests do not tell you about the source of the pieces outside these stretches.

Each of two half-siblings do get half of their autosomal DNA from their common parent.  On average, half of the DNA each gets from that parent will also be inherited by the other half-sibling, and so will show up as matching stretches when the tests are compared.  Thus half-siblings will show around 25% shared DNA (around half of the 50% that comes from the shared parent).

Given a matching stretch of DNA results, one can determine the DNA variants that came from the other, non-shared, parent for the locations within that stretch of chromosome.  However, the locations outside the set of matching stretches cannot be identified with a particular parent (without testing of the parents).

There are two spots on that web page that do get this right.  One is in this diagram:

In the above, the bracketed area does identify the associated parents, but the unbracketed areas cannot be so identified.  (The colors shown are not reported by the DNA tests, so you can't just "follow the color" to identify matching chromosome areas outside the brackets.)

The other spot the web page gets it right is in this paragraph:

  By finding the shared DNA, the brothers can find the pieces of the 23 chromosomes that came from their shared parent, just like we did for chromosome 1.  Any genetic information from the DNA on the corresponding sites on the other 23 chromosomes will tell the brothers about their fathers.

Outside of these two places the web page seems to mislead one into thinking that all the DNA can be associated with the correct parent, which is not the case without the parents being tested.


How does increased heat increase the rate of metabolism?

I don't think a hot shower has any substantial effect on body temperature, since this is carefully regulated by several mechanism to remain around 37$^\circ$C. When you expose the body to heat, you induce a response where the body increases heat loss and possibly reduces internal heat production in order to maintain the core temperature.

It is true that heating the body will increase blood circulation in the skin; this is a way for the body to carry heat from the core to the surface, where it can dissipate (radiate away). As for metabolism, I think the response to heat is less well studied than the response to cold, but presumably metabolic rate (specifically, mitochondrial respiration) will decrease in order to reduce internal heat generation, in order to maintain body temperature. Again, these are homeostatic responses that occur before there is any marked change in body temperature. Here is a review article on these mechanisms.

If you would expose the body to enough heat so that these normal responses cannot compensate, the body temperature will actually rise. Beyond 2-3 degrees (a normal fever), this is very dangerous because it will disturb a number of cellular processes. Cellular metabolism would certainly be affected, but mostly  because some enzymes have narrow temperature ranges where they can function; I don't think the actual heat energy of metabolites is an important factor here, but I don't know of any study on this. A variety of other proteins and cellular structures will be similarly affected. This will eventually affect key functions in the nervous and circulatory systems, which is life threatening. The Wikipedia page on hyperthermia is a good starting point for more information on this.


Could an organism evolve to adaptively evolve?

IMHO, the whole genome replication/recombination/mutation process and arrangement has evolved to increase the likelihood that changes will be beneficial or at least neutral.  In chromosome recombination, for example, new chromosome combinations are constructed from old, tested, gene sequences, while making sure that the new pieces are homologous to corresponding pieces in the parents' and grandparents' chromosomes.


What's the difference between growing cells in culture and cloning them?

Clones are genetically identical daughter cells from one parent cell. So when you start you culture from one cell, all new cells are clones of this cell.
The first three cells (red, green and blue) undergo clonal expansion.

If you multiply cells in cell culture you usually start with thousands of cells, as this can be seen in the second part of the figure. These cells are not genetically identical, as they individually collect mutations. So the daughter cells of each "starter cell" (a lot of them) in the mixture are technically clones, but the whole culture is not seen as clones. See also the Wikipedia on this topic.


Filter proteins by domain with InterProScan

1. Limit the InterPro scan to a specific database:
As you said you know the domain you are interested in so you know which database this is in then you can limit you InterPro scan to that database, which whill save a lot of time:

Then only select the database in which the domain is stored (e.g. ProSite)

2. If your domain is in the ProSite database (which it probably is) you can use
ScanProsite and limit you search to a specific domain.
You do this by going to the above link and select the last option:

Then, if you scroll a little bit down you can enter a ProSite accesion code of the domain/profile you are interested in:

3. Use PFAM scan

I have never used this before, so I don't know whether this would be faster than limiting the InterPro scan to the PFAMa database. You can of course check this out.

4. Clustering your sequences first

This will only work if your sequences look like each other. Depending on the size of the domain and the location in the sequences you can cluster all your sequences first (using for example CD-HIT). And then choose a representative sequences for each cluster and use these to subject to your analysis. For example when you know your domain is always at the end of the sequence then you trim the first part of each sequence and cluster the proteins over the whole length at 100% identity. If you then determine whether each cluster contains the domain or not (based on the representative sequence, which CD-HIT will provide you with) then you can assign these results to the sequences making up each cluster. But of course this will only reduce the search space whenever your sequences look like each other (or if parts do)

5. MOTIF search using downloaded profile or HMM

MOTIF search allows you to query against serveral database, such as PFAM, CDD, PROSITE etc. More interesting, it also allows you to specifiy your own profile or HMM.

So you can download the HMM of your desired domain from e.g. PFAM  or the domain profile from Prosite.

6. Downloading HMM and use HMMscan (or HMMER)
This was suggested by @seven11, you can search your HMM domain in the PFAM database and then use HMMscan.

Conclusion

If you are really interested in one domain. I think downloading the ProSite scan tool would be your best option. Notably, all webtools I mentioned above are available as command line tool, and that is what you need when having that amount of sequences. Back to ProSite scan, you can download this here and don't forget the README. As mentioned in the readme:

Input/Output:
  -e : specify the ID or AC of an entry in sequence-file
  -o : specify an output format : $formats_string
  -d : specify a prosite.dat file
  -p : specify a pattern or the AC of a prosite motif
  -f : specify a motif AC to scan against together with all its
       releated post-processing motifs (but show only specified
       motif hits)

You can use the -p to specify the acc of the pattern you want.

I'm quite busy so I typed this one really fast, please let me know when something is not clear.


Confusion about the construction of the rat's mental map

You have a couple small misunderstandings that I think are making it hard to understand the figure. There is no map of the hippocampus pictured here!

1) Note: this is a schematic figure. These aren't real data, although there are real data that show this pattern. This is meant to be an easy to understand diagram that explains how place cells work.

2) Panel (a) is EXTERNAL SPACE. Essentially it's a "top down" view of a floor that the rat is running around on.

3) Panel (b) shows spike trains for three different cells: theses cells have been arbitrarily color-coded. The hash shows the times that cells 1, 2, or 3 fired spikes. There are just three cells shown in this figure: there aren't any combinations of cells considered one color or multiple cells in one color, just three cells and three colors.

4) Panel (a) is showing how researchers have connected spiking data, like in (b), to the animal's location. The procedure is this:

Start with a blank map of space.
Record from Cell 1. Every time cell 1 fires, mark a blue dot in panel (a) indicating where the animal was when Cell 1 fired.
Record from Cell 2. Every time cell 2 fires, mark a green dot in panel (a).
Record from Cell 3. Every time cell 3 fires, mark a red dot in panel (a).
(the previous steps could be done for many more than 3 cells simultaneously or in sequence; in this example they are just using 3 cells)

5) Panel (c) is in world space, just like in panel (a), and it shows a hypothesized way that the animal could be using the activity of cells 1, 2, and 3 to determine where it is in space. A researcher recording from cells 1, 2, and 3 could also use those recordings to make a guess of where the animal is. If only cell 3 fires within some window of time (an appropriate window is indicated by the outlined ovals in (b) ), and cells 1 and 2 do not, then the best guess is that the animal is in the upper left area that's shaded only red. If all three cells fire, then the best guess is that the animal is in the very center overlapped region of space.

The dashed line shows a hypothetical path the animal might take through it's environment. If the animal took this path, we'd expect to see place cells firing just like they did in panel (b): first only the blue cell, then blue+green, then all three, then red+green, and finally red only.

6) Very importantly: the animal has way way more cells encoding place than just these three. It would be really confusing to plot them all out in discriminable colors like these, but it is this more complex map with thousands of dimensions that gives the animal a good internal representation of its current location.

Hope this helps!


How do cellular waste products enter arterial blood?

Arterial blood isn't "pure". It is simply in one part of a complex circuit which carries varying degrees of oxygen, nutrients, and waste products, etc., to varyious parts of the circuit.

  ...how are these waste materials getting into the arterial blood?

The most simple and direct (but teleological) answer to this is that toxins need to get into arterial blood to ever get to the kidneys to be filtered. The arteries carry blood to every part of the body, detoxifying organs included. Veins carry blood away. If there were no waste products in arterial blood, the kidney would be superfluous.

Waste is produced in all tissue. Blood carries oxygen and nutrients to the tissue (where some of it is used), and via the venous side (all over the body) blood carries the waste products (as well as unused oxygen and nutrients) away toward the heart. The blood carrying waste products collects in increasingly larger veins until it is dumped into the right side of the heart and pumped into the lungs, where a major waste product (CO2) is partially removed. Things that need to be removed by the kidney are all still there. Blood carrying these toxic products is dumped into the left side of the heart, and thus enter the arterial blood supply. The kidney then can remove waste products partially or completely when it reaches them.


Molecular Evolution: Mrbayes never stops?

There are a few things you can try to get better convergence. I'd try the following in increasing order of difficulty/effort/processing time.

Be satisfied with a higher standard deviation of split frequencies. The MrBayes manual says "A rough guide is that an average standard deviation below 0.01 is very good indication of convergence, while values between 0.01 and 0.05 may be adequate depending on the purpose of your analysis." Especially if you are interested only in the best supported parts of the tree, this is a viable option. 0.01 is only a guideline.
Run the model for more generations. Maybe it is on the way to converging, but it hasn't gotten there yet. 100000 is not really that many. Try 200000 or 500000 and see if the model space is still being explored. You can examine the .p files using Tracer. You may already be doing this, and this is why you know it is not converging. If you look at the plots of the log-likelihoods, they will become relatively stable when the run has reached the optimal location.
Try running with a different amino acid model or without the inverse gamma rate prior. If you can get a simpler model to converge, then
Increase the number of chains to 4 or 8. If you have the ability to run in parallel, this will greatly speed up your analyses.
Try iteratively changing the heating parameter by setting Temp to a lower value, which will increase the likelihood of a swap. By default, Temp = 0.1. You can watch the progress of the analysis in the command line and see which are the heated chains and which is the cold chain.


Why did they expect Astronaut Scott Kelley's telomere shortening to accelerate? (they got longer!)

Dr. Bailey wrote a short piece that hints at the reasons behind why she expected what she expected:

Telomeres are the ends of chromosomes that protect them from damage and from “fraying” – much like the end of a shoestring. Telomeres are critical for maintaining chromosome and genome stability. However, telomeres naturally shorten as our cells divide, and so also as we age. The rate at which telomeres shorten over time is influenced by many factors, including oxidative stress and inflammation, nutrition, physical activity, psychological stresses and environmental exposures like air pollution, UV rays and ionizing radiation. Thus, telomere length reflects an individual’s genetics, experiences and exposures, and so are informative indicators of general health and aging...
Our study proposed that the unique stresses and out-of-this-world exposures the astronauts experience during spaceflight – things like isolation, microgravity, high carbon dioxide levels and galactic cosmic rays – would accelerate telomere shortening and aging. To test this, we evaluated telomere length in blood samples received from both twins before, during and after the one year mission.


From the abstract of the linked article (Guttman, 2002):

  We used an in vivo genetic screen to identify 13 effectors [...]. Although sharing little overall homology, the amino-terminal regions of these effectors had strikingly similar amino acid compositions.

And from the body:

  The screen relied on the type III secretion signal and the endogenous promoter of the hop gene and was thus highly specific.

Hence, the authors search and identify proteins with a secretory signal under the regulation of a hop promoter. A functional screen in this paper refers to the analysis of protein samples to detect the presence of proteins with a particular function.


Are there any documented instances of coronaviruses being directly transmitted from bats to humans?

It is possible, but unconfirmed, that the first incidents of SARS-CoV were directly infected by bats, and that palm civits were infected parallelly:

  The new study demonstrates that Chinese horseshoe bats harbor a pair of SARS like viruses that are very closely related to the strain that caused the 2003-2004 pandemic and that these strains have the capacity to directly infect human cells and civet cat cells as well as bat cells. These findings suggest that bats may have directly infected humans and that civet cats may have been incidentally infected.

More Evidence Emerges That Bats May Have Spread SARS, JAMA (2013)


Are neurons clustered? How do neurons make thousands of connections?

In addition to the comments pointing out other inaccuracies, I think the biggest, most obvious misconception that completely invalidates the whole premise is that axons most certainly do NOT have a single terminal; axons branch and make thousands of individual synapses along their length and at the ends of any branches. For excitatory projection neurons in the cortex, for example, the axons can stretch for many millimeters (or centimeters in larger brains), but also typically branch near their origin to contact the dendrites of neighboring cells.

The number of synapses and number of neurons contacted varies greatly across brain areas, species, cell types, etc.

You might be interested in "small world" organization, such as at link, which I suppose could be considered a form of clustering, but it has absolutely nothing to do with the mathematical distance explanation you are proposing.

The only correct equation you can write here is that the spacing S between neuron A connected to neuron B, must be S<=D+L, where L is the length of A's longest axon, and D is the length of B's longest dendrite; for many pairs, S << D+L. These equations will not lead you directly to any valid conclusions of clustering.


Why does squinting allow you to see objects more clearly?

This is an optical pinhole effect.  If the amount of light passed through the lens decreases, the sharper the image is at the focal point.  For a camera this is accomplished by increasing the f stop (f22 is a smaller aperture size than f6 — f-stop is an inverse number).  For the eye the iris will dilate (get larger) or contract to be smaller.  In very bright light, you can cut down on large amounts of light coming in by squinting, which creates a slit in front of the eye lens.

In photography this increases the "depth of field". Which is to say that more objects are in focus and sharp.  It works the same for our eyes of course.

In this image you can see as the aperture is smaller, any given point on the focal plane (right hand line) receives light from a smaller angle (i.e. from less of the image field).

I am not a physicist, but that's a first order explanation
@Luke reminds me that there was a question about whether squinting is harmful.  There is another reason that we squint.  If we are nearsighted or if we are getting older, we have a tendency to squint not because there is too much light coming into our eyes, but because our lenses are not focusing very well.  Is it harmful to strain our eyes?  Maybe, but it won't kill you.  Reading glasses won't either.


Is it possible to breed neanderthals through selective breeding?

No, it is not. As you said only 1-4% of non-subsaharan africans' genome is from Neanderthal and it is more or less the same sequences. The entire Neanderthal genome is not present in modern day humans, it is only a small set of sequences.


Can I make an population genetic analysis from incomplete protein?

It very much depends upon what type of analysis you want to perform. For a Tajima's D, all you would need is a single nucleotide sequences in a sample of individuals, so yes you can. Whether or not the sequence came from a gene or any other sequence is not relevant to whether you can compute Tajima's D (although the type of sequence will likely affect the resulting D).


What is the purpose of THC for a Cannabis plant?

Apparently it is used by Cannabis sativa as a type of sunscreen as it absorbs UV light
https://www.reddit.com/r/trees/comments/2v79dv/science_sunday_13_wait_why_does_cannabis_have_thc/

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


All currently existent forms of life (and all their ancestors) are thought to be descended from a single life form known as LUCA (Last Universal Common Ancestor). Within those organisms, all organisms that share a common ancestor more recent than LUCA are said to be phylogenetically related. These organisms are (ideally - see note) grouped together by scientists into monophyletic taxa.

Therefore, ideally, each taxon represents a group of organisms that have descended from a single common ancestor, not shared by any other taxon. Taxa are defined at various levels including, but not limited to, Kingdom, Phylum, Class, Order, Family, Genus and Species, with organisms at each level having a more recent common ancestor than the ones preceding it. For example, for humans, a superficial phylogenetic classification would look somewhat like this:

Kingdom: Animalia (shares a common ancestor with all multicellular, eukaryotic, heterotrphic, motile organisms)
Phylum: Chordata (shares a common ancestor with all animals that possess a spinal cord)
Class: Mammalia (shares a common ancestor with all chordates that produce milk and are warm-blooded)
Order: Primates (shares a common ancestor with all monkey-like mammals)
Family: Hominidae (shares a common ancestor with all the great apes)
Genus: Homo (shares a common ancestor with relatively recent humanoid species)
Species: sapiens (shares a common ancestor with all humans)

As you can see, this means that all humans share a common ancestor with all other humans, but going further back, they also share a common ancestor with all primates, all mammmals and all vertebrates. Eventually, all animals share a common ancestor, and if you go as far back as LUCA, so does all life.

Note on taxonomy and phylogenetics: Many modern taxa are (to the best of our knowledge) monophyletic, meaning all organisms in a given taxon share a unique common ancestor. However, there remain several taxa that are paraphyletic, because they were described before modern genetic methods became available, or because no one has got down to reclassifying them or (in at least one case, reptiles and birds), because they are so widely used that changing the classification could (and probably would) cause a lot of confusion. So, when using taxonomic classifications to deduce phylogenetic relationships, a bit of caution must be exercised to ensure that the taxon one is talking about is indeed monophyletic.


What is this giant mosquito-like insect?

The better entymologists among us may need to correct me, but I believe you are looking at a robber fly, especially based on the characteristic long, tapering abdomen, as well as the proboscis that reminded you of a mosquito and the large size.
I see a couple people posting images from Texas that look a bit like yours (especially the all-black body) on Google images but none of these mention a genus/species for me to dig further on. Bromley, S. W. (1934). The robber flies of Texas (Diptera, Asilidae). Annals of the Entomological Society of America, 27(1), 74-113. may be useful but is a bit too deep for me to dig into for you.


What makes/breaks the hydrogen bonds between DNA and RNA during transcription?

I wouldn't really say RNA polymerase is "creating" the hydrogen bonds so much as it's thermodynamics that creates them. When we talk about an enzyme "creating" a bond, what we're generally referring to is an enzyme facilitating a reaction by lowering its activation energy so that it can proceed.

However, in the hydrogen bonding between base pairs, there's not really much activation energy to overcome. Before the formation, the nucleotide is just floating around in the cell (solvated by water), and forming a base pair is more energetically stable than not being paired. When a ribonucleotide happens to diffuse into contact with the unpaired DNA strand, the hydrogen bond will spontaneously form because it's energetically favorable. The thing about hydrogen bonds, though, is they're fairly weak, so there's an equilibrium between formation and breaking. When a mismatched nucleotide diffuses into that space, the hydrogen bonding isn't as strong, and it might be in an improper orientation, so it'll diffuse out again. When the correct nucleotide enters, the hydrogen bonds will form spontaneously, hold it there longer, and orientate it properly. This properly places the phosphates for backbone formation, which allows RNA polymerase to proceed with making the backbone.

As for the breaking of the hydrogen bonds, it's the energy released from the phosphodiester bond formation that causes the bonds to break at the other end of the RNA-DNA hybrid. To simplify things a lot, it's kind of like a zipper, where forward translocation of RNA polymerase along the DNA strand is driven by phosphodiester bond formation, which breaks the hydrogen bonds of the RNA-DNA hybrid somewhat mechanically, as the nascent RNA strand leaves through a different channel than the DNA does.

References:

Structural Model of RNA Polymerase II Elongation Complex with Complete Transcription Bubble Reveals NTP Entry Route

Transcription elongation: Heterogeneous tracking of RNA polymerase and its biological implications


How to design an experiment with scent triggered memory recall in humans?

Scents can make memory recalls. We experience this very often, like when we repeatedly smell a good perfume in ,say a shopping mall , and when some person uses it too, we recall the memory of the shopping mall. This hqppens especially when the smell is associated with a very good or very bad incident.

For an experiment, you can expose yourself or someone to a particular smell ,either very good or very bad at any one time, like during examination or holidays for a couple of times. Next when the person again smells the scent he/she will be reminded of the previous exposure.

As regards to how long the exposure is required to trigger recall,it depends upon how strong the smell is (subtle smell takes ponger time) , how good/bad the memory is (very good or very bad memories will be recalled faster) and ofcourse on the memory associativity power of the person.


When did our ancestors switch to a menstrual cycle instead of the estrous cycle?

Menstruation occurs only in most of the primates, and a handful of other mammals. It is tempting to speculate that place the switch to menstrual cycles evolved right after the split between non-menstruating primates (tarsiers and their relatives) and menstruating relatives (almost all others), which is about 63 million years ago.

There are other menstruating animals, so I am not sure if nature reinvented menstruation whenever social conditions required unproductive sex, or menses are in fact a more archaic trait.

I doubt we have material evidence about all these speculations.


Short answer
This is a difficult question to answer. As far as I am aware, asphyxiation results in excitotoxicity, which causes unconsciousness, brain damage and eventually, death.

Background
Asphyxia is a condition of the body that occurs from severely inadequate oxygen supply, or because of excessive carbon dioxide in the body (First Aid and CPR courses). The brain is the organ most sensitive to hypoxia (Medscape). Nerve cells in the brain can survive only up to four minutes without oxygen (First Aid and CPR courses). Consciousness is lost after approximately three minutes (Forensic Pathology). Permanent brain damage begins after approximately 4 minutes without oxygen, and death can occur as soon as 4 to 6 minutes later (Medline). Asphyxial deaths typically involve respiratory arrest with bradycardia / asystole (low heart rate / cardiac arrest) because of the hypoxia-induced dysfunction of the respiratory centers in the brainstem (Forensic Pathology).

Despite the small size of the brain (2% of body weight), it is, however, the largest consumer of total body oxygen (20%) and glucose (25%), which are delivered by 15% of the total cardiac output (Schur & Rigor, 1998).

A lack of oxygen may result in so called hypoxic-ischemic encephalopathy (HIE), i.e., neuronal cell death due to hypoxia. Its pathophysiology is related to the lack of energy because cellular respiration diminishes. This initially causes neurons to stop firing, and eventually in an arrest of cellular functions and cell death. Even sublethal HIE can set in motion a series of toxic reactions that kills injured neurons and even neurons that have not been damaged during the initial insult. Thus, following global brain ischemia, neurons do not die suddenly or all at once. In some of them, damage develops hours or days after the insult. Most neurons undergo necrosis. In some neurons, HIE triggers apoptosis (Neuropathology).

Specifically, energy depletion is believed to result in a failure of the Na+,K+ ATPase, leading to depolarization of the neuronal membrane (Fig. 1). Synaptic function and conductivity cease at this point. Depolarization causes neurons to release glutamate (Glu) into the synaptic cleft. Glu is the most common excitatory neurotransmitter. In small amounts, it is indispensable for neuronal function. In excessive amounts, however, it is neurotoxic. Some Glu receptors, such as the NMDA and AMPA receptors, are non-selective cation-permeable ion channels. Initially, over-activation of these channels causes a passive influx of  Cl- (and Na+) into cells causing osmotic (cytotoxic) edema and rapid death (Neuropathology).

Additional structural damage develops hours or even days later as a result of Ca2+ influx into neurons through NMDA and AMPA receptors (Fig. 1). This delayed cell death is caused by an over-activation of NMDA and AMPA receptors by the excessive release of glutamate, which causes massive influx of Ca2+ into neurons. Ca2+ activates catabolic enzymes (proteases, phospholipases, endonucleases), and also NO synthase. NO is a free radical and other free radicals are generated due to the impairment of oxidative phosphorylation. Free radicals and activated catabolic enzymes destroy structural proteins, membrane lipids, nucleic acids, and other cellular contents, causing neuronal necrosis. DNA damage from endonucleases and mitochondrial injury from free radicals trigger apoptosis (Neuropathology). Collectively, these effects are referred to as excitotoxicity (Choi, 1992). When enough brain cells die, the person perishes with them.

Fig. 1. Schematic showing the excititoxic effects of excess glutamate in the brain. Source: Neuropathology.

References
- Choi, J Neurobiol (1992); 23(9): 1261-76
- Schur & Rigor, Dev Neurosci (1998); 20: 348-357


Is there an example of a new species through mutation breeding?

Definition of species by the criteria of not being able to breed is problematic: e.g., some breeds of dogs cannot breed, due to the differences in their sizes, yet they are the sale species, as could be dhown by artificial fertilization.
Now, if we take any two closely related species and trace their genealogy deep in the past, we run into the same ambiguity: it turns out that at some point they could breed, and their separation into two dustinct species unable to breed was a process that lasted hundreds of thousands ir millions of years.
This brings us to another point: the characteristic evolutionary times for most animals are too long, compared to the existence of our civilization, for dustinc species to appear
This may not be true for faster evolving organisms, such as viruses or bacteria - e.g., HIV had diverged from SIV about hundred years ago. However we cannot define them as different species, except by saying that the dissimilarity if their genetic sequences exceeds certain threshold.


Species Identification - small insect: is this a bed bug?

This is a really old thread but just in case someone happens upon it, this isn't a bed bug.

I am not an expert but it looks like it's likely a book louse or psocid.
See comparison photos of unfed first instar bed bug nymphs vs. psocids/booklice here: http://bedbugger.com/2008/03/04/booklice/
It's all about the shape of the head and body.


Why don't Australian magpies in Tasmania swoop at people?

I cannot give you a proved explanation of why magpies don't swoop in Tasmania. Nevertheless, my goal here is corroborating your impression with some data, and indicating a possible cause.

Aussie Magpies and swooping

Australian magpies are not the same species of European magpies (Pica pica). Actually, they are not even corvids. They belong to the Family Artamidae, and their scientific name is Gymnorhina tibicen (synonym: Cracticus tibicen). Here is a male magpie (you can tell he's a male by the white colour in his back):

Australian magpie in Victoria

Magpies are territorial birds and in the breeding season (which is right now, as I write this, in September) a small percentage of the males become quite aggressive towards people approaching the nest.

According to the Wikipedia link above:

  These magpies may engage in an escalating series of behaviours to drive off intruders. Least threatening are alarm calls and distant swoops, where birds fly within several metres from behind and perch nearby. Next in intensity are close swoops, where a magpie will swoop in from behind or the side and audibly "snap" their beaks or even peck or bite at the face, neck, ears or eyes. More rarely, a bird may dive-bomb and strike the intruder's (usually a cyclist's) head with its chest.

Cyclists are well known targets:

As a personal and anecdotal note, I have to say that I bike during the breeding season and I was never attacked by a magpie, nor I've ever seen a magpie swooping.

No swooping in Tasmania

Your claim sounded quite incorrect to me when I first read your question. After all, the magpies in Tassie (short for Tasmania) and the magpies in the mainland belong to the same species (G. tibicen).

However, after some research, your claim seems to be correct: there is very few, if any, report of magpies swooping in Tassie.

For instance, this is a chart from the Magpie Alert website:

As you can see, there is no registered attacks in Tassie (TAS) from 2013 to 2017.

And here is a map of the attacks (the online version is here):

Most of the attacks happen in Victoria and New South Wales. However, besides Tasmania, you can see both in the chart and in the map that there is no attack registered in Northern Territory (NT) and New Zealand (NZ) as well.

That data doesn't prove that there is no swooping in Tasmania, but it does show that, somehow, Tasmanian magpies behave differently. Maybe they are more shy, or maybe the males over there perform other behaviours to drive off intruders before swooping. It's also possible that the explanation is completely different: maybe people in Tasmania don't like to go online and complain about magpies.

A possible cause

The Tasmanian magpie (G. tibicen hypoleuca) is the smallest magpies of all in Australia. Besides that, it is the magpie that forms the largest groups (Kaplan, 2004), with as many as 15 individuals.

Tasmanian magpie, also a male

Coincidentally, magpies form smallest groups exactly in the areas of higher incidence of swooping, like Victoria and New South Wales. The possible correlation among those variables (swooping rate, body size and group size) is something that is still to be investigated.

Conclusion

However, regardless the actual explanation, the fact is that the number of registered attacks in Tassie is, indeed, smaller than in the mainland. After doing a lot of research, the explanation for this remains unknown to me. Let's wait for more answers.

PS: as I said in my comment, magpies are not that aggressive: they are very nice birds and very intelligent ones as well. So, one way to avoid attacks from the magpies in your area is becoming friends with them: magpies have a good memory and they can recognise a face after years. So, if you become friends with your local magpies, they probably won't attack you if you get closer to the nest. By the way, the best way to making new friends is with food (that works with humans too).

Source: Kaplan, G. (2004). Australian Magpie: Biology and Behaviour of an Unusual Songbird (Australian natural history series). CSIRO Publishing.


How can we tell which direction sound is coming from?

The head-related transfer function. Sound coming from front, and from back differ because of the human body's asymmetry in the vertical direction where the biaural cues such as inter-aural timing and intensity differences are identical. The shape of the ear, and body is necessary for this perception, but eventually, the signal must be analyzed by the brain for localization.


Why have whales and dolphins not evolved to have gills?

I think you're looking at this the wrong way.

Animals evolve to fill niches. Many, many land animals returned to the water as a place to live, including:

  whales, dolphins, porpoises, seals, sea lions, walruses, manatees, dugongs, otters, hippos, pygmy hippos, crocodiles, sea snakes, sea turtles, river turtles, river snakes, etc. etc. etc.

Their success in this environment points to no need whatsoever to "evolve" gills to be better suited. Without the interference of man, there would be yet many more of them.


Why does a light object appear lighter in your peripheral vision when it's dark?

Short answer
Peripheral vision is more light-sensitive than central vision.

Background
When you look directly at an object the image is projected onto the fovea. The fovea has maximal visual acuity (high resolution) and a high density of cones, which are specialized photoreceptors to sense colors. However, cones are not very sensitive to light.

Here is a picture showing the foveal field of view:

Source: Pinhole Eyeglasses

If you look at the same object using peripheral vision, the image is formed more eccentrically on the retina. Here, cones are sparse, but high densities of rods are present. Rods do not detect color, but are much more sensitive to light than cones. In fact, they can faithfully detect a single photon! (Webvision) Moreover, many rods converge onto a single ganglion cell, and rod responses are therefore summated. This spatial  summation further increases light sensitivity in the periphery, but degrades spatial resolution.

Here is an image on rod and cone distributions on the retina, showing a high cone-density in the fovea and a high rod density more eccentrically:

Source: Webvision

And here is an image showing the higher light sensitivity of rods over cones:

Source: Webvision

Hence, peripheral vision is more light sensitive because: (1) there are more rods in the peripheral retina; (2) rods are more light sensitive; and (3) eccentric retinal rod circuitry further amplifies the rod responses. However, color perception and spatial resolution are better developed in the central field of view.

Further reading (Cognitive Sciences.SE)

Rod and cone distributions: "Why can we not see around our point of focus of our eyes?"
Visual acuity as a function of retinal eccentricity: "Visual acuity and offset stimuli"


What is the molecular mechanism of cystine bond formation?

If your question is with respect to a eukaryotic cell, the di-sulfide bridge/bond is formed in the rough endoplasmic reticulum which is an oxidative environment (unlike most other organelles which are reductive). This paper may be of relevance to you:

Pathways for protein disulphide bond formation - Frand et al, Trends Cell Biol. 2000 May;10(5):203-10.


do tumour cells begin with abnormal characteristics?

Cancer cells don't start to become cancerous at a specific stage of the cell cycle; you will find that while uncontrolled proliferation is a hallmark of cancer, different cancers acquire alterations in different phases of the cell cycle. BRCA-deficient cancers for example have a compromised G2-M checkpoint [1], while Rb deficient cancers have a compromised G1-S [2] checkpoint in the cell cycle.

The cell cycle is simply a property of proliferating cells and the same broad phases of the cell cycle are universal to both normal and malignant cells.

As for when abnormally growing cells actually become a cancer - this has nothing to do with phases of the cell cycle, and everything to do with the ability to break through the basement membrane of the original site (indicating the potential to be invasive/spread), because the ability to invade is a hallmark of cancer [3]

References

[1] http://cancerres.aacrjournals.org/content/67/13/6286

[2]  https://www.ncbi.nlm.nih.gov/pubmed/16936740

[3]  https://www.ncbi.nlm.nih.gov/pubmed/21376230


Why do cells vary in shape and function when they have the same genome and the same organelles?

Because cells are not only characterized by by their genetic material and other interior components, but also by the genes they express. Cells have to fulfill multiple different functions to be able to build complex multicellular organisms. Differently expressed genes lead to different proteins made in the cell, which leads to different morphology, shape or function. For example melanocytes in the skin are highly specialized cells which mostly make the pigment melanin. Plasma cells on the other are highly specialised for making antibodies.

It is all about regulation of genes. The RNA doesn't know or transcribe anything -
the DNA is trancribed into the mRNA (which is then further processed) and finally translated into proteins. Cells develop from precursors which proliferate and finally differentiate into highly specific cells. This progress is controlled and activated by specific transcription factors and growth factors. For example: pigment cells only develop, when a specific transcription factor is present. When this factor cannot be expressed, these cells do not develop at all.

This developmental process is shown schematically in the figure below (the figure is from the NIH website on stem cells):


B. Higher surface to volume ratio allows better interface with environment.

C. To increase surface area the cell can form processes such as microvilli.


Can nature create codes and specified complexity?

If you think of laws of nature as being codes, then we've found many instances of such codes that are in some sense not man-made. Of course, you could say that they are of "divine creation" or some such thing, but then you'll probably be ready to label everything seemingly intelligent, interesting or found as such. So let's not go there! These laws can be seen as codes, albeit not intentionally created ones.


What do firebugs do when they "connect" by their rear?

They mate!

These matings can be very long

  When copulating, firebugs (Pyrrhocoris apterus) form tandems for prolonged periods. Half of the copulations of marked individuals in the field lasted longer than 12 h, and some lasted up to 7 days. (Schöfl and Taborsky (2002))

The likely reason for such a long mating is for males to guard the female to prevent future matings and therefore to prevent sperm competition

  males prolong copulations as a form of ejaculate-guarding under high competition with other males. (Schöfl and Taborsky (2002))


What does it mean for a species to be ancient?

It depends on the context.

first "cockroaches are ancient" is different than a species being ancient, cockroaches are not a species but a group of species with a similar morphology and ancestry (similar to a clade).

It can mean they are mrophologically similar to their ancestors. Which is very different than saying they have not evolved. It means the pressures on the linage have not favored much in the way of morphological change. Some shapes just work well,(or reach equilibrium) and once you reach it the morphology don't change much even when other things are changing.
It often means that the split between the lineage in question and other groups is old. example, you could say mammals are ancient for instance because the mammal lineage split off the rest of the amniotes 275 millions years ago. They have changed a great deal since then but the groups as a whole goes back a long time. the issue here is these splits are minor when they occurred, like any other specialization event, but look big due to human constructed categories.
But it can also mean that the lineage has not undergone a specification event for a long time, It has changed but has not left behind any offshoots, this is the rarest case but can happen.

Note however this is a phrase the media like to throw around when it doesn't have a solid scientific definition, it is a qualitative contextual statement. They often have little understanding of its meanings. They also often fail to clarify which they mean, and often fail to properly define the "thing" being ancient.


Can DNA sequencing of food provide quantitatively the fraction of protein from chicken vs soy?

While this question falls somewhat between biology, chemistry, and food science, the use of quantitative DNA analysis as a proxy for estimation of relative protein fractions from two different species (in this case plant vs mammal) is probably on-topic here considering it is biologists who have invented, use, and interpret results of DNA amplification and sequencing analysis, and can best speak to their correct use and potential problems when used outside their accepted protocols.
I am not a trained biologist myself, so I can not state with authority that starting with a food product whose plant and animal components may have started from different places on Earth, been processed differently, then combined and further processed involving major excursions in heat (cooking) and in pH deviate substantially from accepted protocols for DNA quantitative analysis, but I have a strong hunch that this is probably so.
As @BryanKrause has noted in a comment, the laboratory in question's primary expertise is in animal identification - does a carcass or piece of meat or fish come from the species claimed or not, and this is a laudable service. But using relative fractions of DNA within a single sample of prepared food as proxy for relative contribution of protein is far outside that kind of service, and as far as I know, is not an accepted practice anywhere.
Ars Technica is a popular technical news source that generally does a excellent job of summarizing scientific topics when they do cover them, in my opinion at least. In an update to the article Subway releases data after scientists weigh in on 50% chicken test [Updated] they summarize released information from two independent laboratories using an "ELISA methodology designed for food products to quantify soy in the chicken." ELISA is a quantitative method that can be used to measure the presence of various proteins directly, and does not use DNA as a proxy.

Update, March 6: Subway has released the lab reports from both of its independent tests. Both Maxxam Analytics in Ontario, Canada and Elisa Technologies, Inc. in Florida used enzyme-linked immunosorbent assays (ELISA) designed for food products to quantify soy in the chicken. ELISA's are a standard type of assay that generally detect and quantify substances based on binding by an antibody. In the assay, antibody binding kicks off a detectable chemical reaction, commonly resulting in a color change. In the case of Elisa Technologies, the lab used an antibody that binds to soy flour proteins and the lab used known concentrations of those soy proteins for comparison to determine the quantity of soy protein in Subway's chicken samples.
In all samples, Elisa detected 3 parts-per-million or less of soy proteins, which is well below one percent of the chicken. Maxxam detected 5.3 ppm of soy protein in the chicken, which is still well below one percent. (emphasis added)


Did my wildlife camera take a picture of a lynx?

Lynx or Bobcat
Without a clearer image or a better sense of scale I cannot say which. Their silhouette is just too similar.


PhyloCode is not a new system but it isn't popular yet and actually quite opposed by some.
It overlaps with the ranked based systems but does not nullify them, meaning that even if PhyloCode becomas popular the ranked systems will still be needed.
One might understand from your question that virus have no classification system, but they have. The common one is called ICTV.
PhyloCode can classify virus and there is already a classification for virus (ICTV)


Is Norway spruce (Picea abies (L.) Karst.) isohydric or anisohydric species?

This review paper states that spruce is isohydric, citing Physiologie und Ökologie der Gehölze by Lyr, Fiedler, & Tranquillini:

  Spruce appears to reﬂect an isohydric strategy (Lyr et al. 1992), reducing stomatal conductance at early stages of soil drought.

It's important to note that this is not a binary distinction, isohydric and anisohydric are two extremes in a spectrum of how plants respond to drought.


Kinetochore (KT) is a multilayer protein complex. It's main function is to link chromosomes to the positive ends of the spindle microtubules. Also it plays role in the formation of heterogenic region at and around the centromer. The attachment of the KT is not uniform among living species. According to this paper on KT assembly in yeast:

  .  ...  KTs  remain attached to the MTs throughout the cell cycle in this organism. However, a temporary detachment of chromosomes  from  MTs  occurs  (for  1–2 min)  at  the  time of CEN DNA replication in S phase in S.cerevisiae (Kitamura et al. , 2007). After completion of CEN replication, a KT reassembles and reestablishes its attachment with  MTs.

source:http://femsle.oxfordjournals.org/content/femsle/338/2/107.full.pdf
(CEN - centromere, MT- (spindle)microtubules)

Thus the exact time of kinetochore attachment depends on the organism, though I must note that S. cerevisiae has somewhat different mitosis than us.


How does a garlic clove thrive inside a closed refrigerator?

Your garlic was likely purchased as a bulb, not seed, and stored in the fridge.  The garlic 'clove' is not frozen, so your fridge readily mimics underground conditions in the temperate late winter or spring season. The bulb is generally buried underground, and the subsequent initiation of plant development and growth uses the stored energy. In a garden, the garlic would, however, begin photosynthesizing soon thereafter. Bad news: in your fridge, the plant is certain to become etiolated, because the lack of light, and yes, eventually run out of the stored resources--and die. Good news: you can eat or transplant it.


Can blood that has had an anticoagulant added to it be boiled without coagulating?

Coagulation, or clotting, is a proteolytic cascade that generates an insoluble fibrin based protein net, or mesh.

Anticoagulants are things like EDTA (?) that chelate divalent cations required for the clotting cascade.

Boiling blood will denature most, if not all, of the soluble serum proteins, forming an insoluble precipitate.  This is structurally different from a blood clot.

Think about what happens to the white part of a chicken egg when you boil (or heat) it.  That is protein denaturation.


What is the importance of hydrogen bonds in water? and other questions:

You are saying what hydrogen bonds are doing, not why are they able of such achievements, despite being so weak. Their strength is in numbers. At room temperature, fully one fifth of the water molecules are engaged in four bonds with other water molecules, while the remainder forms two such bonds. (More detail at http://www1.lsbu.ac.uk/water/hbond.html ). In contrast, hydrogen sulfide forms essentially no hydrogen bonds with other hydrogen sulfide molecules, despite significant similarity between oxygen and sulfide. The difference in size between oxygen and sulfur makes the former much more electronegative. I could go on with other hydrogen compounds, but the fact that answers your first question is: each water molecule is involved in a series of bonds with other water molecules, on an unequaled scale.

Also, hydrogen bonds are stronger, pickier about distance and angle than the alternatives available to other molecules (dipole-dipole, van der Waals etc.) So even if they seem feeble, and even if the alternatives were as plentiful as hydrogen bonds, the latter would still be more capable of tying up molecules.

The effect of water drying (which comes after swimming, but also after sweating, bathing, or cleaning oneself with a hot oshibori) is caused by water evaporation. Each state transition, including that from liquid water to air-borne vapors, is a heat-consuming phenomenon. When skin dries, the heat to turn water into vapors has to come from somewhere. In perspiration's case, it is one's body.

Note that cooling down while water evaporates is not only something we feel, but a physical reality, occurring even in innate systems. For example, Amazon forests and Sahara are similarly close to the Equator, but the former is cooler than the latter, in part because heat it receives is in part used up to evaporate water.

Your answer was good.

Again, you are right. Were water non-polar, it would have lower latent heat, or, in lay terms, it would evaporate without much heat consumption. Were sweat made of a non-polar liquid, it will fail to consume heat when evaporating, leaving one to warm up sooner / faster.


I think you're going for a view of tube formation, in which case, here's a good image:

Lateral plate mesoderm
Intermediate mesoderm
Somite mesoderm
Chorda
Endoderm

(Reference)

Again in your drawing I think you correctly have it labeled as 10, and don't really need to put it twice.


What are reasons we know insects evolved on land rather than water

The sister group of hexapods (Insects plus Collembola, Protura, and Diplura) are thought to be Remipedes. Remipedes are cave-dwelling aquatic pancrustaceans. The most recent common ancestor of Hexapoda and Remipedia was likely aquatic. But somewhere along the pathway to becoming modern hexapods, after they split from the lineage leading to modern remipedes, the ancestors of modern hexapods developed tracheal respiratory systems that function on land. So the evidence comes from the fact that the extant lineages of insects, close to their most recent common ancestor, including Collembola, Protura, Diplura, Archeaognatha, and Zygentoma are all terrestrial.


What is this part of blastula called and how is endoderm formed?

The blastocoel, as you say yourself, is a fluid-filled cavity (wikipedia) so it has no cells. Fig. 1 shows cellular and non-cellular regions of the blastocyst.

Your questions on the formation of the three germ layers during germination are nicely shown in the illustration in Fig. 2, right two panels.

Fig. 1. Blastocyst. source: wikipedia

Fig. 2. Formation of the germ layers. source: Class Connection


How is respiration an unbalanced equation

The ATP is not actually produced from the respiration. It comes from ADP and free phosphate ions.

The production of ATP in cellular respiration happens in all parts of a series of chain reactions, and you can read more about those here: https://en.wikipedia.org/wiki/Cellular_respiration#Aerobic_respiration


How can a YAC be screened against a cDNA library and a cosmid library of genomic DNA to find a gene?

The YAC contains a segment of chromosomal DNA. By using it as a probe they could screen the cDNA library to find cDNAs derived from that genomic region. This would be done by plaque or colony hybridisation. The cDNA clones thus identified represent the "candidate genes" .

The last step is a little unclear. Clearly they are identifying cosmid clones that map to the segment of interest, but they could be using either the YAC or relevant cDNA clones (could be pooled for this step depending upon their aim) as probes. My guess is that they used individual cDNA clones to find corresponding cosmid fragments so that they could home in on the regions encoding the identified cDNAs.


How is the glycemic index computed from a blood sugar curve?

The AUC of identical dosages of sugar depends on digestion speed because of the rate at which sugar is removed from the blood stream. If sugar exponentially decayed in a first order rate, then the AOC would be the same, but it's save to assume some 0 order mechanisms contributing. E.g. alcohol is mostly metabolized in a 0 order reaction rate: A fixed amount per hour.
Edit: If you take up sugar slowly, it might never reach high concentrations in the blood stream and lead to lower AUC then if taken up fast. Each molecule has a longer lifetime if taken up faster.


Can human mRNA be translated in vitro by prokaryotes?

Short answer: Yes, you can.

Usually these are coupled systems for transcription and translation. For these you clone the gene of interest into a vector which contains a prokaryotic promoter which is then used to generate the mRNA in the tube. This mRNA is then translated in the second step into a protein. This works very well, but the protein is missing the typical post-translational modifications of eukaryotic cells like glycosylations, as these are not existant in the bacteria.

These kits can be purchased of the shelf from the usual biotech companies. Mostly these are based on E.coli cell lysates. They work like shown in the figure (from here):


Luciferase promoter vector over p-AcGFP1-C1 vector

You are confusing luminescence and fluorescence. GFP does not emit light. The abbreviation stands for Green Fluorescent Protein. You need to shine a blue light source at it and it will fluoresce green. The problem is that many organisms have background fluorescence, a cell without any GFP can often have a little bit of fluorescence by itself or contain pigments that mask the signal.

Luciferase assays depend on a chemical reaction which oxidises a molecule (luciferin in the case of firefly luciferase) and photons are emitted.  This is much more sensitive than fluorescence but is also a lot more expensive and usually (but not always) requires cell lysis. It is very rare for a cell to emit light by itself so the background will be a lot lower allowing you to see smaller difference.

There are many reasons to choose one over the other in an assay, if you share a bit more on how you intend to use the reporter you can get a more detailed answer.


Polarized epithelium and localization of ion channels

Well, that's a first for me. I wouldn't have guessed gut cells would have voltage-gated channels.
This article describes voltage-gated sodium channels on both the luminal and basolateral membranes:

Barshack, I., Levite, M., Lang, A., Fudim, E., Picard, O., Ben Horin, S., & Chowers, Y. (2008). Functional voltage-gated sodium channels are expressed in human intestinal epithelial cells. Digestion, 77(2), 108-117.
http://www.ncbi.nlm.nih.gov/pubmed/18391489


You are probably thinking about antivenom using immune serum.
You give the venom to a host animal to induce an immune response, and then purify (to the extent possible) antibodies collected in serum from that animal, and then inject these to the patient to neutralize the venom. You don't use the venom directly.
Isolating components of venom could also allow for screening for molecules that will bind to them strongly and possibly block their action, though I'm not aware of specific antidotes that have been produced this way.


Why does the PR form of phytochrome exist?

First off, "evolution" doesn't necessarily lead the most efficient system for anything - it works with what we already have.  Once something has evolved, it might not go away, if there is no particular harm to having it around. You might take a look at the evolution tag, as other people have asked similar questions about the "usefulness" of biological mechanisms and molecules.
Aside from that, having both isoforms is important for the detecting the color of light. When Pr absorbs red light, it gets converted to Pfr, and when Pfr absorbs far red light, it gets converted to Pr.  The ratios of Pr to Pfr allow plants to determine light levels and adjust their growth accordingly:

Sunlight has a R:FR ratio of 1.2

Light under a canopy of leaves has a R:FR ratio of 0.13

Light under 5 mm of soil has a R:FR ratio of 0.88

A higher proportion of FR light allows plants to detect when they are
shaded. Plants adapted for growth in full sun will display greater
stem elongation when they are transferred to shade.  They also develop
smaller leaves and less branching.  This change is due to greater
proportion of Pr to Pfr.

Seeds of certain plants require red light for germination; FR light inhibits germination.  Many small seeds with low amounts of storage reserves (such as lettuce) show such a red light requirement.
If these seeds they are buried below the level of light penetration in the soil, they do not germinate.
If they are shaded by a leaf canopy, causing a high proportion of FR, germination is inhibited, [as] Pfr is required for germination.

Source: Missouri Botanical Garden


Metabolic efficiency for fats and sugars

This is a very complicated question. You need to rephrase your question to be more specific.

Efficiencies of energy utilization from glucose in the presence of O2 (aerobic respiration) are considered to be in the 40% range. Quite good when you consider that an automobile combustion engine is in the 20-25% range.

There is some evidence that betahydroxybutarate (B-OHB) actually provides more available energy for work than does glucose.  See Paper Here.

However, what is often overlooked is the energy needed to generate B-OHB from fat during ketosis, which results in a net loss in efficiency compared to glucose.

One of my favorite blogs is Peter Attia's "The Eating Academy."  He has a Post that goes into this subject somewhat.

I know this isn't a complete answer to your question, but again, you need to be more specific.

Respiration with or without O2.  Efficiencies in generating ATP from source material or only net efficiencies after the ATP -> ADP.


How do we know the human species arose in Africa?

There are two big prongs of the out of Africa theory or whichever name you wish to call it.

Prong the first: fossil evidence. There are lots of different kinds of protohuman fossils. Homo erectus/ergaster are found all across Europe, Asia, and into Indonesia from about 1.5 million years or so until about 70 thousand years ago, where they stop showing up. Up until 125 thousand years ago anatomically modern humans were only found in Africa. About 70 thousand years ago they start showing up in the Middle East, and then they spread out roughly following these paths. The fossil record shows not-humans or almost-humans (Homo erectus mostly) for millions of years, then humans show up at a certain point and then there's loads of human fossils. This point gets more recent as you get further from East Africa.

Prong the second: genetic diversity. Starting with this paper (not sure if this is behind a paywall but the details are not important anyway) human mitochondrial DNA was compared using restriction enzyme mapping. This kind of mapping is super crude (roughly analogous to grinding pottery into a fine dust and grouping the dusts by color) and the original study was pretty limited by the computers available at the time. Nonetheless, they showed that the most genetically diverse geographical group was Africa, and furthermore that any two people from outside Africa are likely more closely related to each other than any two people inside Africa. Genetic diversity goes down the further away from East Africa you get, matching what you'd expect if humans hadn't been living there long. There have only been (very roughly) 60 generations since humans colonized New Zealand. All Maori people, therefore, are at most 58th cousins. All indigenous Australians are at most 1998th cousins. All Africans are at most 8000th cousins.

More recently we've done proper sequencing on the mitochondrial DNA (actually knowing whats written there) and that's allowed much more precise estimation of this sort of thing, and estimation of the timeframes involved. The genetic evidence backs up the fossil record, by and large. (There are a few interesting examples where interbreeding with Neanderthals and maybe Denisovans can be detected, and that the settlement of the middle east by modern humans about 125 thousand years ago failed. They left no descendants.)

Fun side consideration (warning, extra science, proceed with caution): all humans inherit their mitochondria from their mother, and all males inherit their Y-chromosomes from their father. This lets us trace matrilineal lines with a relatively high degree of accuracy, since mitochondria reproduce asexually. To clarify: your matrilineal line is your mother, and her mother, and so on. Your paternal grandmother is not part of your matrilineal line, nor are your aunts or sisters. These lines are statistically guaranteed to eventually converge on a single woman whose mitochondrial descendants now live in all of us. The reasons for this are complicated. There are actually lots of these women, since she inherited her mitochondria from her mother, ad infinitum (well, not infinitum. Ad failed-endocytosis-of-an-alpha-proteobacterium-leading-to-mitochondria doesn't roll off the tongue though). Science has tight estimates on the most recent mitochondrial ancestor, or "Mitochondrial Eve". To be clear: there were loads of other women alive at the time, and we inherit a lot of their non-mitochondrial DNA. Over millennia all those other women had fewer daughters, and their matrilineal lines died out. She lived about 200 thousand years ago, plus minus 20 thousand years. As a mathematical guarantee we'll never find her body or have a really tight estimate on how long ago she lived, but she's genetically guaranteed to exist. The same principle applies to patrilineal inheritance, but the estimates for the most recent ancestor of all Y-chromosomes are a little looser (200-300 thousand years ago). See here for a more detailed handling of Eve and what's going on there.

In sum: old fossils only in Africa, everyone outside Africa is only 2800th cousins with each other or less, but intra-African relatedness is less than half that (more than twice as far away genetically).


According to LeRoy G. Holm's World Weeds: Natural Histories and Distribution:

  Seeds are protected from germinating in the stalk by the swelling of the pistillodes that are distributed throughout the inflorescence. In humid conditions, they swell and keep the spike intact. They can swell 15 to 20% in 15 min in 100% relative humidity. Upon drying, the pistillodes shrivel, air again reaches the seed, and the perianth hairs spread. Their collective pressure causes the inflorescence to burst, releasing the fruits to the air. If they fall on water, the hairs close and the pericarp releases the seed which then sinks.

So it's all about the humidity!