What are the most popular theories in a nutshell?

To date, the mechanism of action of paracetamol is not fully understood. There are some experimental evidences, but it is difficult to put things togheter. It is now clear that  paracetamol acts contemporaneously via at least three pathways:

The inhibition of cyclo-oxigenase (COX)

The main mechanism proposed is the inhibition of COX, it's highly selective for COX-2.
COX are molecules involved in the metabolism of arachidonic acid (aa). It catalyzes the reaction to form prostaglandin H2, a pro-inflammatory compound, from aa.
Paracetamol, as other NSAIDs,  block this step , thus reduce the amount of prostaglandin H2. The reduced amount of prostaglandin H2 in the CNS, lowers the hypothalamic set-point in the thermoregulatory centre.

The exact mechanisms by which COX is inhibited in various circumstances are still a subject of discussion.

Some authors state that paracetamol works by inhibiting the COX-3 isoform—a COX-1 splice variant—of the COX family of enzymes.
This variant is expressed mostly in brain, so it is the one supposed to be involved in the antalgic effect of this compound.

There is another physiopathologic possibility to explain its action, that is: paracetamol would block COX, but in an inflammatory environment where the concentration of peroxides is high, paracetamol itself is oxydated and thus inactive. When it founds a non inflammatory environment, such as CNS, it become reduced and thus active (it reduces temperature, it has anti-dolorific action, etc).

The modulation of the endogenous cannabinoid system, through its metabolite AM404, a compound that inhibits the reuptake of the endogenous cannabinoid/vanilloid anandamide by neurons.

The COX model can explain quite well the action of paracetamol, altought it has been demonstrated an important role of the endocannabinoid system aside of COX. When cannabinoid receptors are blocked with synthetic antagonists, paracetamol's analgesic effects are prevented.  This is tought to be due by an active metabolite of paracetamol, that is called AM404 and inhibits the reuptake of anandamide.

Anandamide reuptake lowers synaptic levels of anandamide. This results in a more activated pain receptor (at least the main one, called TRPV1, or according to an old nomenclature: vanilloid receptor). The high levels of anandamine, due to inhibition of its reuptake, desensitise this receptor in a way similar to the capsaicine.
Furthermore, this active metabolite (AM404) inhibits sodium channels, this chemical behaviour is shared with lidocaine and procaine, two common anesthetic drugs.

These two actions by themselves have been shown to reduce pain, and are a possible explanation of paracetamol's mechanism of action; but one other specific activity of this compound remains unexplained by these two models.

Serotonin receptor agonism.

It has been observed that this compound can reduce the social rejection in humans. This can't be explained with COX or type I endocannabinoid system modulation.
Increase of social behavior in mice dosed with paracetamol, wich models a reduction of social rejection response in humansdoes not appear to be due to cannabinoid receptor type 1 activity. .
In the animal model, it seems a result from  serotonin receptor agonism.

Aside of this main features, some other evidences are in bibliography.

In 2011 a debate started on scientific journals. Some has found  a hint to the analgesic mechanism of paracetamol, being that the metabolites of paracetamol e.g. NAPQI, act on TRPA1-receptors in the spinal cord to suppress the signal transduction from the superficial layers of the dorsal horn, to alleviate pain.
This findings has been contested in a  new hypothesis paper  on how paracetamol might act.
This second study concedes that NAPQI is the active metabolite but that this reactive compound should react not only with the thiol in TRPA1 but also with any other suitably available nucleophile that it happens to encounter. This broad interaction with thiol groups in cysteine proteases, like the ones that process  procytokines, might be the targets giving rise to overall analgesic effects, changing the global cytokyne environment.
Even if there are evidences of drug-body interaction with formation of active metabolites and there are some models of drug action, many things are not fully cleared and the debate is still open.

  Why are they a popular theory?

Are popular because are based on experimental and clinical evidence. Also, this theories can model lot of the biological effects of this compound.

  Which protein is targeted?

Not any time it can be possible to reduce a pharmacological interaction at this level. For instance, in one theory it inhibits an enzyme, the cyclooxygenase (COX); in one other model entire classes of molecules, the sodium channels, are modulated...
Unfortunately many times, dealing with living organisms, it is not possible  to offer an hard, mechanicistic explanation of things.

  How does that inhibition introduce the analgesic and antipyretic properties?

In the COX inhibition model, the analgesic properties can be explained trough an affinity for COX3; and the antipyretic activity can be due to the reduced amount of prostaglandin E2 in the CNS, in the thermoregulatory centre it lowers the hypothalamic set-point. The endocannabinoid model can explain preety well the anti dolorific actions, as well as the serotonin receptor interaction the behavioral one.

  Is it possible multiple theories are correct?

Yes, there is a substantial overlap between different regulatory systems, so that is straight to think that the same chemical (or some of its different active metabolites) can modulate different systems.

  Why is so little known about paracetamol? Is it exceptionally difficult, or the norm in pharmaceutical research of relatively old effective drugs? If it ain't broken, why fix it!

Is it not that difficult topic! One can say that is as tricky as any clinical pharmacology topic. The problem is that many compound are clinically used as drugs even if their molecular functionig is unknown if they are safe and of proved usefullness. This is true for paracetamol as well as many other drugs, like a lot of anaesthetic agents as Propofol.


Why are plant cells rectangular and animal cells spherical shaped?

Animal cells

Generally all (animal) cells have different shapes because they do different things. Each cell type has a specific role which it has to play in order to assist the body in working efficiently and functionally. Thus their shape supports them to carry out these roles effectively.

Look at (animal cells):

Neurones
Photoreceptors
Immune Cells

Plant cells

They are often square shaped/rectangular because it is easier to build a "brick wall" (cell wall) out of rectangular bricks.  Any structure that minimises interstitial space will hence allow more "life", thus possibly making it stronger.

This is also due to:

  Plant cells are not necessarily square, but they due tend to have distinct edges and be somewhat rectangular. This structure is caused by the cell wall which is very rigid and therefore forces the cell to have a defined shape.

However there is one exception I could think of, and those are pavement cells, they're neither round nor somewhat spherically shaped. Pavement cells are a cell type found in the outermost epidermal layer of plants.

Sources:

Beckett, B. S. Biology: A Modern Introduction. Oxford: Oxford UP, 1976. Print.
http://www.academia.edu/3786570/Plant_Cell
Rappaport, R. Cytokinesis in Animal Cells. Cambridge: Cambridge UP, 2005. Print.
http://biology.about.com/od/cellbiology/ss/plant-cell.htm
https://www.msu.edu/~whymerky/CellS&Funitplan.htm


Are there inherent problems in simulating marine environments, as compared to terrestrial systems?

It probably depends on the type of marine organism you're referring to, some will be much more hardy than others and some will not be able to adapt to change at all. Due to the vast scale of the environment that marine fish come from it's likely that in their natural habitat the conditions they live in are not subject to drastic changes in water chemistry or temperature [1][2]. So recreating those exact conditions for them in man-made habitats, let alone maintaining them is going to be extrememly difficult.  Also, if you think about the conditions that most (there will be some exceptions) terrestrial animals and plants have to deal with on a day-to-day basis they have to be able to cope with some fluctuations in humidity, temperature, weather, light etc and therefore are highly adaptable by necessity.

Other issues can be supplying the correct feed. In artificial settings food may have to be a non-natural substitute and this will likely cause problems for species who require a highly specialised diet. The terrestrial animals we tend to cultivate extensively are omnivorous/herbivorous which are not difficult needs to meet. On the other hand a fish from the sea that requires a particular other kind of fish only found in a particular area and that needs very specific conditions to thrive is going to be problematic.

Check out this article http://www.vliz.be/imisdocs/publications/301.pdf , it might be for a specific fish but it highlights some of the general issues i think you are referring to.

[1] http://www.bestfish.com/saltg.html
[2] http://www.aquaticcommunity.com/marineaquarium/
(both general articles on keeping marine fish)

hope this helps!


One flybase gene number (FBgn), many Affymetrix Id's

I can answer this - I may not have time to dig though the file you are pointing to... but here's some explanation - lmk if you need more.

The shorter names (123456_at) are the original names for the probe sets that Affymetrix gave.  The file you area asking about has been extended for FlyBase's purpose and I'm only dimly aware of its existence. It looks like Flybase has tried to rename the probe set to a minimal gene list and create less ambiguous mappings.  I'm not familiar with it.  If I have time Ill try to look at it and put something here, but I'm fairly slammed this week.

In general you should know, there is a many to many relationship between probe sets from arrays and genes.

There are a few reasons for this.  The most common reasons:

More than one probe set per gene
1) More than one start sequence per gene. The IVT arrays such as you are looking at read only the 3' end of the gene.  If there are  more than one such terminii, you will have more than one probe set.
2) Duplicate genes.  If the 3' end of the gene has been duplicated recently, then a probe set may read more than one gene and not be able to distinguish them, so it will have both gene references in its annotation files.
3) Duplicate probe sets. For older arrays, this did happen where the probes in two probe sets will be mostly or entirely the same.
4) formerly separate genes are now joined into a single gene.  This is similar to (1) above, but with the added reason that two neighboring transcripts seen separately at the time of the array design are currently known to be part of the same transcript.  This is something we often don't think about, but the array may have been designed before your current gene of interest had a full length sequence.

In several cases the transcription behavior of the two probe sets will be quite different and you can decide which one to take based on how it behaves experimentally.  for example one of the probe sets may never respond while another one may register large changes with biological sample conditions.  Sorry I can't be of more help here. There are too many possible scenarios to consider to write about cogently.

More than one gene per probe set
1) a single stretch of DNA, even on the same strand, may simply be associated with more than one gene and the probe set will read both of them.
2) Even if they are not exactly the same, some genes resemble each other in nucleotide sequence that is impossible to choose probes which do not read both of them.

Since they have similar read length to a probe set, all this is also true to some extent for short read NGS sequencers in RNASeq data.

As you can hopefully see, ambiguity is something you have to expect to some extent when deciding to work with a biological system.  In many cases (~ 80%) you will have a single gene read per probe set, but with those odds you'll be looking at the genome browser for a half dozen of your favorite experimental results.


Which landmark paper first described the differentiation of T-cells?

This paper appears to be a history of the discovery of B/T differentiation and the role of the thymus. I believe that you should find a number of important references therein.
It describes specifically a series of publications in the 1950s and 1960s that may be relevant (section "Identification of T and B cells"), such as this one by Gowans.


Up to date, extensive documentary about dinosaurs?

Try Planet Dinosaur (2011) or Dinosaur Revolution (2011). Neither is as good as the original Walking with Dinosaurs trilogy, but both are relatively informative and entertaining at the same time.


Could light/occasional smoking strengthen the lungs?

From your examples only the first is really true. Exercise leads to better physical abilities (within some boundaries).

Sunlight on the other hand is always potentially dangerous, depending on the dose. But the damages accumulate over the years which finally lead to the so called senile lentigos (others call them aging spots) occuring in sun exposed skin from the age of 50.

And the same is true for cigarette smoke. Here you expose yourself to a nasty cocktail of potentially harmful to cancerogenous substances (tar, polycyclic aromatic hydrocarbons, benzene, nicotine and much more). These do potential harm to your lungs depending on the dose (meaning how many cigarettes you smoke a day), but there is nothing like a harmless amount. Your lungs will eventually recover from this (tar takes the longest to be removed), but it is definitely not good.


The sign agrees. They are petunias. The specific variety of the red ones is raspberry swirl. I don't know the specific variety of the purple ones.


How do single-celled predators chase other cells?

Detection of and movement according to a gradient of a chemical species is a strategy that single cells use to track a target across space. There are very many strategies of movement depending on the cell and its environment, but a common problem that while cells can sense the concentration of chemicals, they cannot sense its gradient (the direction in which it increases) because they are of too small a size to rely on the difference of concentration on one side and the other. Howard Berg and his co-workers have discovered a mechanism that allows single cells to move toward increasing concentration zones by a combination of concentration sampling and movement. See his webpage, http://www.rowland.harvard.edu/labs/bacteria/projects/track.php


The odor comes from urea. Urea will slowly undergo displacement to become ammonia, but when it's fresh, it has a strong odor. Other odors do come from food, notably coffee and (in some of the population) asparagus.


What's the mechanism for pain-induced swoon?

Swooning, fainting otherwise termed Syncope or Primary shock (Triggered by pain or any unpleasant stimuli through the vaso vagal effect), is due to generalised vasodilation. The capillaries loose their tone and dilate resulting in an increase in volume capacity of the vascular system. This results in draining of blood to the dependent areas due to gravity thus hindering blood supply to the brain which shuts down and results in collapse (fainting) of the individual. This is a safety mechanism. Once the patient is in the lying down position the blood supply to the brain returns and the patient recovers. An individual who has fainted should not be propped up as this may result in seizures or worse.


Does homology of a trait necessarily imply that the most recent common ancestor had the trait?

Yes, assuming you treat the term strictly.

The term homologous implies that the most recent common ancestor had the trait, although it would be possible for the term to be used in error, when something thought to be a homology is actually not.

If the trait is shared but the trait evolved separately twice, instead you would refer to it as an analogous trait rather than homologous; analogous traits are often the result of convergent evolution.

I can imagine some edge cases, however, where one could argue about homology, although I don't have a specific example in mind (maybe someone can help me out if they can think of one). Imagine you have a trait that is present in an ancestral population, becomes minimized in a common ancestor, and then multiple species descending from that ancestor start to exhibit the trait again. This is called atavism. In some ways, atavism could be seen as convergent evolution and an analogous trait: each has separately evolved that trait from the last common ancestor. However, one would expect a lot more genetic similarity than other examples of convergent evolution and therefore outside of cladistics it might be more appropriate to think of it as a homologous trait in that you can find some ancestor that shared the trait, it just doesn't happen to be the most recent one.


Why does hair turn grey or white, and why does it happen later for some?

Each individuals hair colour is determined by the particular pigment they produce (called melanin - the same stuff in your skin that makes you tan).

As the body ages this pigment (produced by the melanonocytes - cells that reside in the hair follicle) is produced less and less, until the hair is no longer coloured, and appears grey.

This is unique to each individual because it is a genetic (and therefore highly heritable) trait. Because it is in no way linked to mortality there is no selection pressure against greying hair.

The reason that the pigment is not longer produced is the gradual depletion of the stem-cell pool with age. This is common to many tissues, hair follicles being just one. As the 'pool' of stem cells is depleted, the melanocytes are no longer replaced as frequently, and thus less pigment is produced as we age.


What differentiates neurons in different parts of the brain?

During development of the brain neurons undergo several steps of differentiation. They transition from neuronal progenitors to mature neurons, resulting in different types of neurons, characterized most prominently by their primary neurotransmitter. During the differentiation, different genes are expressed, which in research is used to label specific cell types (to e.g. observe their distribution in the brain). Since timing is important in development and neurons migrate to their side of action, later born neurons often display different features than earlier ones. The final differentiation is also dependent on the environment, meaning surrounding cells can influence the outcome.

Not just neurotransmitters, also other surface molecules, types of synapses formed, morphology and many other genetic differences influence neuron function and their diversity. Each brain area has many different neuronal cell types, some are similar between brain areas, while others might be very specific to one area. As an example, there is a microRNA, expressed in only 6 neurons of the nematode worm C. elegans, that is essential for their specific function to sense CO2 by repressing other genes (publication).

Taking the example of your question, here is a paper on the diversity of GABAergic neurons in the amygdala (there are several different types of neurons having the same neurotransmitter but expressing otherwise specific markers, which results in different specific functions in the circuits). The author compares them to GABAergic neurons in the cortex (including hippocampus), where a similar function might be taken over by a different cell type (expression profiles are distinct due to different lineages and environments and can be labeled by different markers).


What's a good reference for choosing histological staining chemicals?

If you want to go way back, google books has Methods in Plant Histology (Chamberlin, 1905) with a PDF. It details stains and the tissues they are used for and even has a section titled "Selection of a Stain."


Temperature affect pretty much all metabolic pathways. There are incentive in fishes as well to control their internal temperature.

Control of Body temperature can be categorize along two axes, one concerning the source of heat and the other the magnitude of temperature variation. Please have a look at this post to understand the terms endo-, exo-, poikilo-, homeo- terms.

Below is a figure to give a general overview of the diversity of species in terms of temperature regulation.

As you can see fishes are found in different parts of the figure.

So, yes there is incentive in fishes to control their internal temperature and to avoid extreme heat as well as extreme cold.


What are some examples of undirected weighted networks in ecology?

Epidemiology, the spreading of diseases, is probably one of the most famous applications of network theory in biology, going all the way back to John Snow.

A more relevant example would maybe be something like graph models of habitat mosaics. Populations are often both spread out over landscapes and clumped together in smaller pockets of suitable habitats. While fragmented, these populations still have a certain amount of contact, resulting in gene flow and the creation of what is often called a meta-population. These things can happen on a vast range of scales, from your back yard to whole continents, but by modeling them like graphs they can all be studied comparatively and tested for resilience agains disturbances, habitat loss etc.

You mention social networks, but there is no reason why you can't study the same in animal populations. Say one individual learns something useful, maybe the location and route to a rich feeding ground. That information can then be shared with other individuals, either by show-and-tell, or maybe by some kind of abstract communication. The information spreads in familiar exponential fashion until everyone knows, then any one of those individuals can relay or be "eaves dropped" on by a neighbouring population, it doesn't even have to be the same species in some cases, and the information flows again. As with the habitat mosaics the benefit of these models is that very different systems can be compared and tested on an equal footing, anything from fish, to birds, mammals, even some social insects, lend themselves well to this.


Is each blade of grass an individual plant or not?

Each blade of grass is part of the grass plant and may have multiple blades.  Clumping grasses, when mature, can spread producing multiple shoots with additional blades.  The number of blades would depend on the type of grass and individual seed, but the clumping grasses tend to produce 10-16 leaves/blades.

Source: Poaceae - Wikepedia


I hope I understood your question correctly.

I think what you are missing is that after you break up the DNA, you dilute the concentration so that each bacteria will incorporate ~1 DNA molecule. Then, you dilute the bacteria on a plate and spread it so that they each single bacteria is far from other bacteria. Finally, after they grow you get one genetically identical colony per DNA fragment.


How are mitochondrial ATT (Ile) start codons translated as Methionine?

The key point in understanding non-AUG start sites in mRNAs is the nature and role of the initiator tRNA.

There is a special initiator met-tRNA which differs in structure from all the elongator tRNAs in such a way that it — and only it — is recognized by the IF-2 type initiation factors (and not by the EF-Tu/EF-1 elongation factors). In a complex with the initiation factor and GTP it can bind to the ribosome at the P-site. Normally the ribosome will also be interacting with an AUG codon at the P-site, but in some cases it is not, so that initiation may still occur.

  Thus, the initiating amino acid is always methionine, regardless of
  the codon, because methionine is the only amino acid with which the
  initiator tRNA can be charged.

In the case of bacterial mRNAs, it has long been known that about 10% start with other codons, predominantly GUG. This can be explained by their relative position to the ribosomal binding site on the mRNA — the Shine and Dalgarno sequence. I imagine this is what happens in mitochondria.

In the case of eukaryotic cytoplasmic mRNAs, an initiator met-tRNA complex normally scans from the 5ʹ-end, initiating at the first AUG or first the first AUG in an ‘appropriate context’. The precise definition of an appropriate context is unclear, and on can imagine that in some cases such a context pauses the ribosome at a non-AUG codon, at which initiation begins.

References

“The Biochemistry of the Nucleic Acids”, 11th edition, Chapter 12 (1992) RLP Adams et al. — this has all the older original references, but not the recent ones.

Wikipedia entry on Shine and Dalgarno sequence.

Eukaryotic scanning model: Hinnebush review (2011)

Initiation in prokaryotes and eukaryotes Londi review (2015)

Related SE Biology Answer on initiation and elongation met-tRNAs (by me)


Why are plasmid genes not already incorporated into bacterial chromosomes if necessary for stressful situations?

Plasmids do have the advantage that they replicate independently of the cells chromosome and that they can be transferred between different bacteria. This spreads the gene encoded by the plasmid to other bacteria, which then can also survive.

Think about antibiotic resistance. Bacteria which have a plasmid which allows protection against the antibiotic will survive. They can transfer this protection to other bacteria which then also become resistant. This can either happen through pili which develop between bacteria or also via the uptake of plasmid DNA from the environment in a process called horizontal gene transfer.

Additionally mutations on the plasmids are not as dangerous on the plasmids than on the chromosomal DNA, where essential genes might be damaged. Plasmids can also get lost, if they are not needed by the bacteria due to a missing selection pressure, which is also much harder for genes encoded on the chromosome.


What is the right definition of 'Sex Linkage'?

Linkage is the tendency of two genes present on the same chromosome to be inherited together. The degree of linkage depends on the distance between the two genes, i.e two genes that are physically close are less likely to be separated onto two different chromosomes during recombination/crossover.

So this is what your first definition trying to convey.

Sex linkage simply means that a gene is to be found on the differential region of a sex chromosome (and not an autosome). See it as (gene) Linked to sex chromosome.

Note: Linkage and sex linkage are not the same.

An Introduction to Genetic Analysis, 7th edition makes it a bit easier:

  Sex linkage is the location of a gene on a sex chromosome.

So to sum up the definition:

  Sex linkage is the location of a gene on the differential region of a sex chromosome. (this is applicable to human beings because we have PARs)

For animals in general having sex chromosomes the definition from Genetic analysis is alright.

Note: Sex chromosomes are chromosomes that have genes that have roles in determining the sex of an individual of a species.


Axons grow but that is not same as cell is proceeding through cell cycle. Cell grows in size but there is no cell division. It is still arrested. However during this process some growth related genes are upregulated which are also upregulated in actively dividing cells.


Pull down mostly refers to immunoprecipitation, however pulling down can be done using other interactions such as streptavidin-biotin or His-tag-Nickel.

In a protein pull-down a protein is enriched along with the molecules bound to it. When the DNA that is bound to a protein is studied, the experiment is called ChIP (Chromatin ImmunoPrecipitation). When other proteins that are bound to a given protein are studied then the experiment is called Co-IP.
Similarly RNA bound to protein can also be studied.

It is also possible to pull-down an RNA or a DNA fragment using complementary oligonucleotide, streptavidin, antibodies etc and study their interacting partners.

In the linked paper, they have immunoprecipitated a HA (haemagglutinin) tagged protein using an anti-HA-tag antibody (Note that this is just a small tag of 9-10 amino acids and not the entire HA protein. Such tags are useful when you don't have the antibody for a given protein).

They have done both co-IP and ChIP:

  HA-tagged, full-length PfSET10 protein and interacting proteins from
  3D7/PfSET10HA and control line 3D7 were purified using anti-HA beads

  Chromatin Immunoprecipitation (ChIP) and Transcriptional Profiling

  ChIP analysis was performed as described (Flueck et al., 2009).

Coverage is a term used in sequencing experiments which usually refers to average number of reads that map to any locus; this is also called depth. This is commonly used in RNA/DNA sequencing studies (See this post too). In this paper, as mentioned in the other answer, the term coverage is used for peptide reads (analyzed by mass spectrometry) and it is the horizontal coverage not a vertical coverage. Horizontal coverage refers to the fraction of actual molecule (DNA/RNA/protein) covered by the assembly of reads.

Coverage has got nothing to do with the pull-down assay; it is used in the context of the downstream experiment.


Would chimpanzees and humans normally be in the same genus if we weren't so sensitive about it?

I have not seen any research that synonymizes Pan and Homo, but that doesn't mean someone hasn't tried to propose it in the literature at some point.  The proposal to synonymize the two genera of course would need to be based on accepted techniques and not emotion (such as just having a particular fondness for chimps).  And such a synonymy would necessarily synonymize all the ancestors that existed since the most recent common ancestor of humans and chimps, or a new structure for the evolutionary relationships would have to be proposed.

I think it's important to note that while there is a right answer when it comes to the structure of the evolutionary history of species, there are no right answers when it comes to naming conventions.  The names exist for our convenience.  Phylogenetic trees themselves which show evolutionary relationships are utilized for other research such as understanding the evolution of traits.  So I don't know if this researcher is thinking there is some need to re-evaluate the structure of the relationships between humans and chimps for the sake of advancing science, or if he's just trying to get his opinion across and/or cause discomfort.

Related posts

How could humans have interbred with Neanderthals if we're a different species?
Does it make sense to classify all humans in a single species?
Is there a consensus on whether or not race exists on a biological level?
Do humans have enough biological differences to be grouped into races or subspecies?


Is there a consensus on whether or not race exists on a biological level?

Anatomically modern humans are less than 200K years old, left Africa (or possibly Africa and Arabia) only 60K years ago, and migrate quite a lot (think of the Mongol invasion).  So you would not expect to have clear divisions into subspecies.  And indeed a quick search of google scholar pulls up no claims in the literature for human subspecies of anatomically modern humans (i.e. no subspecies of homo sapiens since Neanderthals and Denisovans).

On the other hand, it's certainly the case that you can work out a rough phylogenetic tree of humans.  Native americans are descended from certain northern and eastern asians, and so in the 1400s were more closely related to them then they were to other humans.  Similarly, Austronesians (of Indonesia and Polynesia, e.g.) are more closely related to Taiwanese aborigines than they are to Australian aborigines.  This tree is complicated by how much more migration there has been in the last 1000 years than there was previous to that, but it's still biologically meaningful.

But here's the striking thing: traditional notions of "race" do not match up well with this tree.  The deepest and most fundamental phylogenetic splits in the human tree are within Africans.  If you were going to try to "scientifically" come up with races, you'd end up with something vaguely like one for Khoisan, one for other Africans, and one for all non-Africans.  Even ignoring modern admixture, traditional races are not monophyletic.  Any clade including all "black" people includes all people, any clade including all "east asians" includes all native americans.  (Also note that traditional notions of "race" are not stable over time, remember that "Irish" used to be a "race" on the US census.)

Modern admixture even more clearly shows the non-genetic nature of traditional "races."  One genetic study of people who identify as African-American, found that African ancestry can be as low as 1% and as high as 99%, with the median African-American having 18.5% European ancestry (with 30% having European y-dna).  Furthermore, relatively ancient admixture (for example, in the Northern Africa, Northeastern Africa, Middle East region or in Madagascar) also complicates the situation significantly.

To summarize, although human genetic diversity is a real biological phenomenon which can be used to figure out the geographical history of people's ancestors, traditional notions of race do not match up well with the biologically meaningful concepts.


Both strands have a 5' and 3' end. Some genes will be on one strand and some on the other. The coding sequence will always be 5' to 3', but RNA polymerase reads the template 3' to 5' to polymerize mRNA.


Why doesn't CAS9 cleave the original CRISPR sequence in the bacterial genome?

It is not the methylation status. The crRNA is not only complementary to the spacer sequence within the CRISPR array but also to the repeat sequence flanking that spacer. The additional base pairing of the sgRNA with the repeat prevents a nucleolytic cleavage by Cas9. In addition, the arrays typically do not contain PAM sequences.

Here you will find a nice illustration:


In Pigliucci (2004) (repeated in Hansen (2006)) the mutational variance is defined as being the new additive genetic variance entering in the population each generation due to mutations.

In consequence the mutational variance is not define at the level of the mutation in the sense that we do not care about how many mutations yield to this new genetic variance. So none of the suggestions of possible answers in the OP's question is correct.


Much of it is not readily digestible. According to this chemical analysis:

  Finally the results presented here also indicate that the amount of digestible carbohydrates in aquafaba is minimal. For families with GLUT1 deficiency, where a diet with minimal amounts of glucose and carbohydrates digestible to glucose is required, aquafaba can represent an additional foaming or emulsifying ingredient, as an alternative to eggs.

It also contains proteins, presumably digestible. The carb and protein content is significant, according to the study, which implies a fairly decent proportion of undigestable carbs.


Serotonin - Does being aroused make you sleepy?

According to this article [1], serotonin (5HT) inhibits sexual arousal:

Dopamine is generally facilitative to male sexual
behavior; however, 5-HT is regarded as inhibitory.
Antidepressants of the selective serotonin reuptake
inhibitor class (SSRIs, including Prozac and Zoloft)
impair ejaculatory/orgasmic function and frequently
inhibit erectile function and sexual interest as well.

However, serotonin can also facilitate erections:

Systemic administration of the 5-HT1B receptor agonist
anpirtoline impaired ejaculation in male rats. On the
other hand, stimulation of 5-HT2C receptors with mCPP
impaired ejaculation but facilitated erections in male
monkeys, suggesting an increase in parasympathetic
influence.

Serotonin release also causes sleepiness after ejaculation in males (source):

5-HT is released in the LHA at the
time of ejaculation and promotes sexual quiescence during
the postejaculatory interval

There are many signalling molecules used by the human body that have a different effect depending on the cell type they are detected by and the receptor type they activate.
I would also like to touch on your question about evolutionary benefit. Evolution does not care about you after you have reproduced. As long as an individual reproduces, evolution is "happy". For example, you think falling asleep after sex is counterproductive on the evolutionary scale? What about Mantises where the female will sometimes eat the male during or immediately after copulation. Falling asleep seems like a pretty small thing compared to that (source):

Although the praying mantis is known for its cannibalistic mating process in actuality it only occurs 5-31% of the time. Especially in laboratory conditions of bright lights and confinement, the female is more likely to eat the male as means of survival. "In nature, mating usually takes place under cover, so rather than leaning over the tank studying their every move, we left them alone and videotaped what happened. We were amazed at what we saw. Out of thirty matings, we didn't record one instance of cannibalism, and instead we saw an elaborate courtship display, with both sexes performing a ritual dance, stroking each other with their antennae before finally mating. It really was a lovely display". (7) There is one species, however, the Mantis religiosa, in which it is necessary that the head be removed for the mating to take effect properly. (5) Sexual cannibalism occurs most often if the female is hungry. But eating the head does causes the body to ejaculate faster. (3)

Anything that makes an individual less likely to reproduce will be selected against. Things that happen after reproduction do not affect the survival of the species and will not be subject to selective pressures.
References

E. M. Hull, J. W. Muschamp, S. Sato, Physiology & Behavior 83 (2004) 291 – 307


Confusion regarding the Kir2.1 inward-rectifying potassium channel

Short answer
"Inward rectifying" doesn't mean "only allows inward current". Current through inward-rectifying channels can be (and often is) entirely outward in physiological settings.
Explanation
For a non-rectifying channel, there is a linear current-voltage relationship. If you plot current through the channel at various holding voltages, you get a straight line.
For inward-rectifying potassium channels, you get less current as you depolarize, like this:

(from Wikipedia)
At negative voltages, the channel is pretty linear and strongly inward (negative). However, at more positive voltages, the linear trend is attenuated.
However, this relationship does not upset the equilibrium potential for a given ion. For a potassium channel, if you have a cell with a potassium reversal potential that is more negative than the membrane potential, you'll still get an outward flow of potassium ions (in the figure, note all the lines above 0, representing voltages more positive than the potassium reversal potential; they're positive/outward even if they're small). What is different for the inward-rectifying channel is that as you depolarize the cell, the current does not increase the way you would expect it to increase for a non-rectifying channel.
For example, for a non-rectifying channel, you'd expect with a potassium reversal of -90mV, the current would be the same magnitude but opposite sign at -120 mV and -60 mV (30 mV above and below reversal). For a inward rectifying channel, you will still have the same change in sign, but the magnitude will be less at -60 mV than at -120 mV.

its inhibition will allow for depolarisation

Any channel permeable to some ion (or combination of ions) will tend to move the voltage towards the reversal potential for that ion/ions. So, as long as potassium reversal is more negative than threshold, all potassium-only conductances are inhibitory, whether they rectify or not.


You may not want to know. It really depends on how good your math background is.

  A topological crossover is a class of representation independent operators that are well defined once a notion of distance over the solution space is defined [1].

Let's first start with the definition of Topology.

  Topology is the mathematical study of shapes and topological spaces. It is an area of mathematics concerned with the properties of space that are preserved under continuous deformations including stretching and bending, but not tearing or gluing. This includes such properties as connectedness, continuity and boundary [2].

Later on in the paper they start to mention transverse topology which leads to Differential Geometry.

  In mathematics, transversality is a notion that describes how spaces can intersect; transversality can be seen as the "opposite" of tangency, and plays a role in general position. It formalizes the idea of a generic intersection in differential topology. It is defined by considering the linearizations of the intersecting spaces at the points of intersection [3].

To understand the underlining math concepts of this paper, you may need a rigorous background in mathematics. I would check the authors backgrounds to see if they are Physicists or Mathematicians.

Most students in mathematics generally take two courses in introductory real analysis and at least one course in abstract algebra before taking topology. The standard book for a first course in topology is by Munkres.

A book you may want to look into is Topology in Molecular Biology. However, the author is a mathematician, so if you are not, you may need to start with courses in analysis, topology, differential geometry before you tackle this book. I have never seen the book so I don't know how difficult it will be but here is the about the author from amazon:

  M.Monastyrsky is a professor of mathematics and theoretical physics
  at the Institute of Theoretical and Experimental Physics, Moscow, Russia,
  graduated the mathematical department of Moscow state university(1967),
  author of numerous papers in diferent fields of mathematics and
  theoretical physics including the monograph :Topology in Gauge Fields
  and Condensed Matter (Plenum,1993 ) and two other books:Riemann,Topology
  Physics, Birkhauser, Boston, 1999, 2nd ed. and Modern mathematics in the
  light of Fields medals, AKPeters, 1997.I gave invited plenary talks on
  many conferences and was the visiting professor of many universities
  and institutes including IAS(Princeton), Harvard, Princeton and Yale
  Universities (USA), Cambridge and Oxford Universities (Great Britain),
  IHES and Universite de Paris (France).


What flower is this grown in Southern China

Google images sais that it's a mexican petunia, I think it's right due to the good focus of your image, and the different attributes of the photo.

http://www.gardenality.com/ImageViewer/?id=2116&IUID=3&RID=88#imageId=2116


Why do flowers naturally reproduce with their own species?

The pollen from a given species of flower does get transmitted to other flowers of different species (like you said, through air, insects, etc.)..the problem though is that those two species of flowers are just that!: they are two different species, and by definition, aren't able to reproduce amongst one another.

I would recommend looking into the definition of a species. There isn't a single, blindly-conformed-to definition, however, its most commonly accepted that a species can be defined by the "boundaries" in which that species can or can't produce offspring with other organisms. Organisms that can produce offspring together are generally considered to be of the same species.

There are odd cases though where some interspecies reproduction occurs, such as a donkey and a horse producing a mule. Yet, if two mules were to attempt sexual reproduction, they wouldn't be successful in producing offspring (mules are sterile). So, this is a tricky situation to define, in terms of if the donkey and horse are the same species or not, since they can produce offspring, yet that offspring is a dead-end, so to speak.

A different example.. if (somehow) a chicken attempted sexual reproduction with a pigeon, the sperm would reach the females egg, however, no offspring would occur.

A major impedence of offspring occurring for interspecies reproduction comes down to the mechanics of meiosis, and how chromosomes match up with each other throughout the process. Chromosomes need to be of similar size, shape, etc., in order to properly pair with their complement during meiosis. Also, the correct number of chromosomes need to be present. These dynamics, as well as many others, get messed up when interspecies reproduction is attempted.

I hope this addresses your curiousity.. All the best!


I am surprised Janeway's Immunobiology is not listed here:

Murphy K. Janeway's Immunobiology. 8th ed. New York: Garland Science; 2011.

It is very comprehensive, accessible and goes beyond any graduate course I know. Most immunology researchers I know have a copy of this handy somewhere in their office. A particular highlight are the very clear illustration.

I would suspect that a new edition is currently in the works, so I recommend checking if a new edition is due to come out before you buy.


Reflexes & Pathologies including the Vagus Nerve

One pathology affecting the vagus nerve is autonomic neuropathy which can be secondary to several causes-one of the most commonly acquired cause is diabetes mellitus. It can manifest with various symptoms such as resting tachycardia (heart beating fast without exercise), exercise intolerance, orthostatic hypotension, constipation, gastroparesis (delayed gastric emptying), etc.

If you'd like to read more-http://care.diabetesjournals.org/content/26/5/1553.full

Hope its helpful.


Molecular feedback mechanisms create rhythmic patterns. The circadian rhythm is driven by a handful of genes, which in turn can regulate a number of downstream factors.

Here is a very nice explanation of the Drosophila circadian clock, which gives you an idea how this works. The video shows the same animation adding more factors every time to guide you through how the system works on the genetic/protein level.

A brief summary: The genes period and timeless are transcribed over night. Their proteins stabilize each other and build up in the cell. At the same time they block their own transcription, limiting the amount of proteins.
Other factors destabilize the proteins and evoke their degradation. One of them is the light activated protein Cryptochrome. This helps entraining the clock and results in the removal of Period and Timeless protein during the day. The negative feedback of their blockage is removed and transcription starts anew at night, when Cryptochrome is inactive.

These clock genes do not only regulate themselves but can also activate or deactivate other factors resulting in daytime-dependent transcription of genes or protein activity.

The whole picture is of course a bit more complicated and involves a lot of additional factors. But also in humans and other mammals you find very similar mechanisms.


Hardy weinberg equilibrium and Wright Fisher model

Welcome to Biology.SE

When you talk about the 'Wright-Fisher model' I suppose you are referring to the 'Wright-Fisher model of genetic drift (WF)'  involving the use of a binomial distribution.

You are correct that the two models make very similar assumptions. However those assumptions are generally speaking found in a large set of different models just because they often simplify the math. I think it is quite wise to consider these two models as very much independent.

Shared assumptions

Both the WF and the Hardy-Weinberg model (HW) assume

non-overlapping generation
panmictic population
absence of selection, migration and mutation
random mating
no sex-ratio bias

Of course, violation of some of these assumptions are relatively easy to model but such complication is often not taught in intro classes to population genetics.

Wright-Fisher model derivation

Let $2N$ be the total number of haplotypes, where $N$ is the population size. I here just assumed a diploid population but derivation for a haploid population is just as easy. Let $k$ be the number of occurrences of allele A, so that the frequency of the allele A is $p=\frac{k}{2N}$. Assuming sexual reproduction only, the number of occurrences of the allele A in the next generation is

$$k' = {2N \choose k} p^k (1-p)^{2N-k}$$

Quick side note: Effective population size

The variance of this distribution is $var(k') = 2N p (1-p)$. The variance of the allele frequency in the next generation is therefore $var(p') = var(\frac{k'}{2N}) = \frac{1}{4N^2} var(k') = \frac{2N p (1-p)}{4N^2} = \frac{p(1-p)}{2N}$.

Replacing $N$ by $N_e$ and solving for $N_e$ yields

$$N_e = \frac{p(1-p)}{2 var(p')},$$

which is the definition of the effective population size $N_e$.

Wright-Fisher model assumptions

The WF does not per say assume a finite population size, it is just that when the population size is infinite, the model loses all of its appeal!

Hardy-Weinberg model derivation

See here for a more complete discussion

The derivation of Hardy-Weinberg genotype frequencies is simple enough to not rely on any pre-existing model. Let's consider the simple version of the HW model, the one with a bi-allelic locus. The two alleles A and B exist at frequency $p$ and $1-p$ respectively. Imagine you have to draw an allele from this population. The probability to draw a given allele is equal to its frequency. Now draw a second allele. Assuming the population is large enough or assuming that selfing is allowed, the probability of drawing a given allele is still the same at the second draw than at the first draw.

As such the probability of drawing the allele A twice is simply $p p = p^2$. Similarly the probability of drawing the allele B twice is simply $(1-p)(1-p)=(1-p)^2$. The probability of first drawing the A allele and then the B allele is $p(1-p)$ and the probability of first drawing the B allele and then the A allele is $(1-p)p$. If we don't make the discrimination between AB and BA genotypes and just call them all AB, then the frequency of the AB genotypes is $2p(1-p)$. Of course $p^2 + 2p(1-p) + (1-p)^2 = 1$.

Hardy-Weinberg model assumptions

It is common to say that HW assume infinite population size. This is correct if you make from HW the interpretation that the genotype frequencies are exactly at $p^2$, $2p(1-p)$ and $(1-p)^2$ and that no evolutionary change will occur. But if you interpret HW as indicating the expected genotype frequencies from which deviation exist, then you do no make the assumption of infinite population size. Under this second interpretation, one can test deviation from HW expectations with a binomial test (or most often, when the population size is large enough with a $\chi^2$ goodness-of-fit test).

Related post

Solving Hardy Weinberg problems is very related and offers a good tutorial.


Examples of extant animals in a submature morphologically unstable evolutionary state?

Not sure exactly what you're looking for, but maybe the Giant Panda is of interest to you. The Giant Panda is an herbivore, but it has evolved from a meat-eating animal (the most recent common ancestor of Pandas and the other bears). It made the switch from omnivore to herbivore just ~2 MYA. According to wikipedia, pandas still have the digestive system of a carnivore. They can still eat meat and do not actually get much protein/energy from bamboo. Thus, you could consider them to be in a state of evolving from an omnivore into a more efficient herbivore


OK, I know this is old, but here goes. The tail current is the current at -55mV after the voltage step, here:

The current shrinks as the voltage changes, this causes a massive shift in the driving force for the ions either side of the cell membrane. Going from -125 to -55 mV for the largest step. As commented, the dense vertical bands either side of the step are due to fast capacitance readings, basically ignore unless you want to go down a whole other avenue.

The reason for the tail currents is some channels remain open and close gradually after the step ends "tailing" off. We can't really say what channels these are as we know nothing about the recording conditions/cells involved. However these currents are large, so most likely to be sodium/potassium.


What does the difference between GPP - NPP represent?

The answer is in your overview: it's plant respiration.

  Is the value of 800 equal to respiration?

That is the unavoidable consequence of the equation you presented and the numbers you plug in, yes.

  I understand that GPP is the overall rate of biomass production by producers at the rate at which solar energy is captured as carbohydrate molecules during photosynthesis and NPP (energy captured per unit error per unit time).

That sentence was fine until "and NPP". What is it doing there? Did you misquote something or are you thinking NPP is a process like photosynthesis?

  Producers such as plants use this energy respiration and growth.

Yes.

  I also understand NPP is the rate of energy lost to metabolism or maintenance or the energy stored as biomass by plants or primary producers in the ecosystem.

No. NPP is the energy stored as biomass by plants or primary producers in the ecosystem (or rather the rate at which such energy is stored, if it's productivity you're talking about and it's in gC/m-2/yr-1). Respiration is the energy lost to metabolism or maintenance. GPP is what that sentence seems to be describing, as it's the total carbon captured by plants, i.e. whether it's used to build up the plant's biomass or used by the plant in its metabolism (i.e. respired).

  I am making the assumption that this value of 800 is associated with the respiration of plants;

Correct.

  although, I am still confused with what this value represents.

Maybe you should study the metabolic processes of plants and life in general to better understand this. All life consists of chemical reactions that build up structures; in order to build them up you need energy (because of the second law of thermodynamics), and all living things create that energy by breaking down complex molecules into simpler ones. (as such it would be more accurate to say that all life consists of chemical reactions that build up and break down various structures). You might be wondering "but what about the difference between autotrophs and heterotrophs I heard about"; the difference between those is where they get the complex molecules from in the first place. Autotrophs use a different source of energy to build them up while heterotrophs get them from their environment. As such, you can think of every living thing as being made of two kind of molecules: those that actually form their structure (in humans, the molecules that make up cell membranes, bones, muscles, etc) and those that are stored in order to be broken down to power the whole system (in humans that's fat, glycogen, glucose, etc). Of course a molecule can do both; if you're starving your body may start to break down structural molecules for power. There are many different ways of breaking down those big molecules for power; the most efficient one, that starts with a big chain of carbon atoms and cuts it down into individual CO2 molecules using O2 molecules, is called aerobic respiration (i.e. respiration that uses oxygen).

Because those complex molecules are required to power all life, autotrophs (the organisms that actually make them) are very important, and the processes they use to make them are very important too. The process that makes almost all of the molecules that power almost all life on earth is photosynthesis, which uses the energy from the sun to power a reaction that converts CO2 from the atmosphere into big carbon-based molecules we'll call carbohydrates. This is called "fixing carbon", since the carbon atom is the most important one; measuring how much photosynthesis is happening is another way of measuring how many carbon atoms move from being part of a CO2 molecule to being part of a plant.

GPP is the measure of that exact process: how many grams of carbon per square meter per second (or year in your graph) move from being in a CO2 molecule to being part of a plant via the process of photosynthesis.

You might think this is also a measure of how much the plant grows, but it ignores the fact that as I said, all living things contain molecules that make them up and molecules they break down for power; obviously the plant's growth will involve the former, and the latter just goes back to being CO2 through the process of respiration. Another way of putting it is that in the flow of carbon, there is a huge flow of CO2 to plant molecules via photosynthesis (GPP), but a huge proportion of that flow goes right back the other way (the plant molecules are broken back down into CO2 via the plant's respiration); the remaining flow that's actually still in plant molecules at any given time is NPP.

NPP is the proxy for plant growth; it's basically how much of the carbon the plant fixed via photosynthesis it actually contains in its body, while R (respiration) is how much of the carbon it fixed it broke back down for energy, releasing it as CO2 into the atmosphere. Hence, GPP = NPP + R, and GPP - NPP = R.

  From my way of thinking, the difference between GPP-NPP equals the extent of CO2 lost from plant respiration within the ecosystem.

Indeed.

  Since the value of GPP (1400) is larger than the value for NPP (600), more energy has been used during the intake of carbon during photosynthesis rather than plants using glucose or the energy stored in the system to photosynthesise for the emission of CO2.

I don't understand this sentence at all. The fact that GPP is larger than NPP shows that plants don't keep all of the carbon they convert from the atmosphere to make up their physical structure; they also use a lot of this carbon to power their metabolism through the process of respiration, which results in said carbon turning back into CO2 and being released back into the atmosphere (as opposed to staying in the form of wood, leaves, starch, etc).

  Therefore, this value represents the amount of CO2 that is lost from plant respiration or from metabolic activity.

That is correct, with the two caveats that it's the amount of carbon fixed in organic molecules that is lost by being released into the atmosphere under the form of CO2, and that there is no "or" - all plant metabolism is fuelled by respiration, and the only metabolic activity that releases CO2 is respiration.


What causes the variable/conserved structure in the 16S rRNA gene?

The structure of ribosomal RNAs involves double-helical stems, on the one hand, and loops or junctions, on the other. A comparison of small-subunit rRNAs of different sizes shows that, despite increasing complexity, a basic core structure exists. The is illustrated in the diagram below is adapted from Brimacombe, Trends in Biochemical Sciences (June 1984) 273–277.

From a structural (3D) point of view, both stems and loops are conserved, but as far as the nucleotide sequence is concerned, the helical stems are less conserved than the loops and junctions. This would appear to be because the main function of the helices is structural — so an A–U base pair can generally be replaced by a G–C (or U–A or C–G) base pair, whereas the loops are involved in interacting with various species — tRNA, initiation, elongation and termination factors, ribosomal proteins and the 50S subunit — which may involve more specific bases.

The main thrust of research on ribosomal structure (and what has interested me) is the relation of structure to function, but Carl Woese realized that, because of its ubiquity, rRNA was an excellent molecule for phylogenetic studies. Although, if one compares, say, mitochondrial ribosomes with mammalian ribosomes the sequence conservation is small, with different strains of bacteria it is much larger. This has led microbiologists interested in bacterial phylogeny to analyse the best regions for comparison in 16S rRNA, in terms of their degree of conservation, resulting in the concept of variable and conserved regions in the diagram in the question. (I find this terminology rather unfortunate because of its similarity to the totally unrelated immunoglobulins.) It appears that this is due to van de Peer et al. (1996), from whose paper I reproduce the figure below.

[Figure 3 of van de Peer *et al.*The most variable positions are in red, the most conserved in blue. Absolutely conserved positions are indicated in purple. Nucleotides present in E.coli but absent in >75% of the bacterial sequences considered are indicated in pink.]


Air purifier agains bacteria and viruses?

The aforementioned filter will filter microbes

Yes, it is routine practice to use microfiltration in labs to sterilize solutions from microbes. 0.2 micron filters will remove all typically-found bacteria most of the time, except for the odd bacteria here and there, though this is uncommon. 0.1 micron filters certainly remove all stray bacteria that may make it through upon a single 0.2 micrometer filtration. Here is a nice read on the appropriateness of 0.2 and 0.1 microfilters, which simply states that 0.2 micro filters are usually more appropriate since they additionally guarantee a better flow rate.

The aforementioned filter will NOT ensure filtration of viruses

These filters are not used, suitable nor effective for viruses, however. You ask specifically about the coronavirus. From a 2015 study:

  Coronaviruses are members of the Coronaviridae group and contain a
  single-stranded, positive-sense RNA genome surrounded by a corona-like
  helical envelope (Ryan 1994). The SARS virus genome consists of 29,751
  base pairs. Approximately 41% of the genome is GC base pairs while 59%
  is TA base pairs. Coronaviruses have a size range of 0.08-0.15
  microns; with a mean size of 0.11 microns (see Figure 1).

This means 0.1 micron filters will not protect you from these viruses. They may help you reduce viral count in the air, which may of course be sufficient, but this would not be an adequate measure in a biological safety facility.

The cost-effectiveness of commercial air-purifiers for biosafety vs. pollution

On a advice-related note: I do not think air-purifiers are going to help you in a cost-effective manner to avoid viruses (e.g. Rhinoviruses that cause the common cold, for instance), lest you stay at home all the time. You expose yourself outdoors, and carry plenty of viruses indoors on your body and in your respiratory tract; these will bypass your filtration system on the daily. Being healthy and lucky enough to avoid exposure to viruses outside the house is still the best bet. I think an air purifier has a greater potential to help with smog and urban pollution, those particles are typically larger than the diameter of most microbes.


How is SARS-CoV-2 'deactivated' for some Covid vaccines (for example Covaxin)?

For Covaxin (BBV152), SARS-CoV-2 was inactivated by treatment with β-propiolactone [1]. β-propiolactone reacts with and modifies, among other things, nucleic acids, thus preventing their replication [2].
[1] Yadav P, Ella R, Kumar S, et al. 2020. Remarkable immunogenicity and protective efficacy of BBV152, an inactivated SARS-CoV-2 vaccine in rhesus macaques. Preprint.
[2] Perrin P, Morgeaux S. 1995. Inactivation of DNA by β-propiolactone. Biologicals 23(3):207-211.


Why do mountain gorilla eat just 1.7% fruit, while lowland gorillas eat 25%?

Mountain plants have to be hardy, especially if they grow above the frost line. They are more likely to be tough vegetation (leaves, shoots, and stems) as mentioned in the mountain gorilla diet.

The lowlands have much more plant diversity (and generally better food). Sweet fruits have better calories for the effort required to forage and digest them, so you would expect the lowland gorillas to prefer fruit.


Neanderthal and modern human population sizes

Briggs et al. 2009, using mtDNA report an estimate of 3500 females. They failed to offer any estimate of the male population size. Their estimates is much  lower than previously thought. They report two hypotheses of why their estimate is so low:

Hypothesis 1 - Low population size

H. neanderthalis population size was indeed really low. After all, they mostly had to live in harsh ice age conditions.

Hypothesis 2 - Slow decline in population size

H. neanderthalis population size were quite high at some point and their population size slowly decreased in size up to the point of being completely wiped out. Such low decline in population size may explain the low level of genetic diversity observed (yielding to an estimate of small population size) in their sample. If the decline of H. neanderthalis was sudden, then even the last survivors of the lineage would have shown quite a high level of genetic diversity. Their decline may have started about 40,000 years with the arrival of Homo sapiens in Europe but this is just a speculation. This second hypothesis is congruent with the evidence of a rather rapid rate of evolution observed in H. neanderthalis

In short, we don't really know what the population size of H. neanderthalis was but it might have been as low as 3500 females only


This paper uses a similar technique to you by purifying total RNA, synthesis of double-stranded cDNA containing a T7 promoter sequence, cDNA purification, in vitro transcription in the presence of biotin-labeled ribonucleotides and this transcription is possible with T7 RNA polymerase since the cDNA contains the T7 promoter region, and finally fractionation of RNA. This then allows target biotin-labeled RNA for short (~ 25 nucleotides) oligonucleotide arrays. The T7 polymerase performs a linear amplification, and the in vitro RNA obtained reflects the abundance of each transcript in the initial RNA.

Hence I assume you follow a similar protocol although I'm not sure why you do RT-qPCR on the fragmented RNA since that is unlikely to work if you are doing it using primers for specific regions as everything is fragmented. So I think you do a RT-qPCR before the fragmentation to test the expression levels of certain (known) genes (to see if you are getting the expected results) before you go ahead with fragmentation and look at the global RNA expression. If my assumptions are wrong, then it would be great if you added further details of your experimental protocols with the different steps and the exact orders of the steps followed and the results assessed and the experiments performed so that I can modify my response.


Why does crossing over take place at all?

Crossing over is believed to be beneficial for evolution. It does not cause only mutations, it allows for the switching and mixing of genetic information. Thanks to crossing over entire protein families evolved, like the hemoglobins. Indeed it is one of the mechanisms that shaped the chromosomes.
Some in-silico simulation proved that, in general, adaptation take place faster if crossing over is applied.

Here some extra references for further readings.

https://www.ncbi.nlm.nih.gov/pubmed/28565671

https://www.ncbi.nlm.nih.gov/pubmed/28564047

https://www.ncbi.nlm.nih.gov/pubmed/28563027

https://www.ncbi.nlm.nih.gov/pubmed/28557225

https://www.ncbi.nlm.nih.gov/pubmed/28555659


Can more than one antibody bind the same antigen

Let's clarify the terms. An antigen is a molecule that can be associated with a particular substance (virus, pollen, dander.) When an immunoglobulin or antibody recognizes an antigen it binds to a specific epitope. An antibody recognizes an epitope using its paratope.

Some antigens have multiple epitopes; this means that different antibodies can simultaneously bind to them (if the epitopes are far-enough apart from each other so that binding to one doesn't preclude binding to the others.)

An example from my work is influenza (flu) hemagglutinin, which is a major viral coat protein. Here's a low-resolution structure showing a "head-binding" antibody fragment (actually three of them), and here's a similar structure showing a "stem-binding" antibody fragment. Our immune repertoire (and physiology) greatly predisposes us towards producing head-binding antibodies over stem-binders. Note that each structure has three antibody fragments bound in the same state. Because the head-binder and stem-binder antibodies are well-separated in space they can both be accommodated in a single complex (as is experimentally confirmed.) In this case, up to six antibodies, using two distinct paratopes, could simultaneously bind to a single antigen.

For matured (high affinity and high specificity) antibodies, each binds a specific epitope. The typical state of affairs is then explained "one antibody per epitope" which is overly simplistic because some epitopes can be recognized by multiple paratopes (which would be found on different antibodies.) So a given epitope can be recognized by no antibodies (a new antigen, or one that is poorly immunogenic) or by multiple ones.

  Is it true to say that the same substance could bind with (and, therefore, be recognised by) more than one antibody, or not?"

Yes, that's true.


I presume it is a female Dolichovespula adulterina living in the Palearctic (Austria and Germany) and Nearctic regions.


Why does ostrich meat look and taste more like beef than chicken?

There is a very plausible explanation here.

Basically, it explains that meat colour is due to the protein myoglobin (a haem-containing protein related to haemoglobin). There are two types of skeletal muscle: fast-twitch and slow-twitch (Wikipedia). Slow-twitch muscle is red muscle because it contains lots of myoglobin. Fast-twitch muscle is white muscle, containing less myoglobin. The Wikipedia link explains a little more about these muscle types and their functional differences. Evidently the lifestyle of the ostrich dictates that it have more fast-twitch muscle, and so it has red meat. It isn't unique in this: duck and goose are classified as red meat too.

Incidentally the role of myoglobin is to improve the rate of diffusion of oxygen from the haemoglobin in the capillaries through the cytoplasm of the myocytes to the mitochondria. It has also been suggested that it acts as an oxygen storage mechanism in diving mammals which have very high levels of myoglobin in their muscles, but this storage function is unlikely to be important in other mammals, despite what you may read in textbooks.


How does Mupirocin affect in staphylococcal infection?

This comes from the usage of the Mupirocin: Its an antibiotic, which is used topically (on the skin, its not taken in form of pills). It binds specifically to the isoleucyl t-RNA synthetase in gram positive bacteria and Streptoccus and Staphylococcus and is used to fight intranasally (that what i/n stands for) infections with these bacteria. It inhibts the introduction of isoleucine into proteins. More informations can be found here.


The term 'functional' in this context implies a type of analysis that is able to provide a mechanistic understanding.

The authors first describe their exploratory approach, by which they identified some genes and their mutations that are associated with patient relapse in acute lymphoblastic leukemia. Then they proceed to intervene in the system, by expressing mutated KRAS in mice. When they did that, they observed several hallmarks of relapse in those mice. Hence they can conclude that a mutation of this gene is involved in the mechanism that underlies relapse.

Thus the way these authors use the term 'functional analysis'/'functional dissection' is in contrast to a correlational approach.

The underlying assumption is that by isolating parts of the system and studying their properties and their effects we will be able to understand the physical world. This is a philosophical (metaphysical) thesis called reductionism, which is arguably the prevailing view in the natural sciences.

The first use of the term "functional dissection" I could find is in a 1971 paper on the immunological response of small molecules. Their goal in that paper was to dissociate (or dissect) the effects of small molecules, such as a bovine glucagon, on antibody specificity versus antibody production. They have found that different parts of this molecule were responsible for antigen specificity (all antibodies recognised the N-terminal) and cellular immunity (mostly the C-terminal of the molecule was associated with DNA synthesis).


If coelocanths are more related to humans than groupers -does a Coelocanth's DNA literally have more sequences in common with a human than a grouper?

Yes, in virtually every way. In terms of pairwise distances, measured in percentages, humans and coelacanth are closer to one-another than coelacanth would be to any ray-finned fish. In terms of individual genes, there would be genes that humans and coelacanth share with their common ancestor, but are not found in any ray-finned fish. Remember, humans are bipedal terrestrial fish.


Is it still true that C. elegans has no known natural viruses?

It has a natural virus, an Orsay virus.
https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1000586
is the paper of the discovery. found by searching "virus infecting C elegans"


What are the costs associated with carrying lots of genetic material

It is generally known that the smaller (or less complex) an organism is, the more "condensed" it's genome is. For example, bacteria (or some eukaryotes) have operons (http://en.wikipedia.org/wiki/Operon) or overlapping genes using different and they don't have introns, which alltogether saves a lot of space.

There are many reasons for that. Available space in the cell is definitely not one if it, however. Energy for copying and maintenance is a good point, but you have to keep in mind how evolution works. Bacteria and unicellular eukaryotes are usually adapted to a very specific environment in which they can reproduce rapidly. This means, they only need a small set of genes, specific for this environment and they have to reproduce very frequent, which means they are very prone to mistakes during DNA-copying. Such a mistake can lead to the death of the cell, which in this case equals the death of the organism.

In higher organisms however, the advantages of a bigger genome outweigh the disadvantages by far. Evolution can happen much faster because and mistake while copying does not necessarily lead to the death of the whole organism. Adaptation to a much greater variety of conditions is also necessary, e.g. when you look at plants: Their genomes are (on avarage) much bigger than the ones we mammals have, because they cannot move if the conditions around them become unpleasent. Instead, they need to find a way to adapt. This means, a big genome is in this case a fitness bonus. More interestingly, plant genoms are highly mutable (http://en.wikipedia.org/wiki/Transposable_element), which was originally thought to be a huge disadvantage.


How much does calcium reduce iron absorption?

In short: Calcium can inhibit absorption of iron, but this does not necessary have any significant effect on the long-term iron status in the human body.

Iron (Linus Pauling Institute):

  The presence of calcium decreases iron absorption from both nonheme
  (i.e., most supplements and food sources other than meat, poultry, and
  seafood) and heme sources (meat). However, calcium
  supplementation up to 12 weeks has not been found to change iron
  nutritional status, probably due to a compensatory increase in iron
  absorption. Individuals taking iron supplements should take them two
  hours apart from calcium-rich food or supplements to maximize iron
  absorption.

In various studies, calcium from food or supplements in usual amounts decreased iron absorption by about 50%, but the calcium dose/iron absorption relationship cannot be simply quantified, because it is affected by several factors, for example:

Phytates in food inhibit the absorption of both calcium and iron (BiomedCentral).
Calcium may inhibit the absorption of nonheme iron from plant foods less than heme iron from meat (academic.oup.com).
Different calcium supplements may differently affect the absorption of different iron supplements.

The inhibitory effect of calcium on iron absorption is not linear and one may not be able to express it as a simple formula. Below are some examples from studies.

A review of studies, American Journal of Clinical Nutrition, 2010

  The reported dose-effect relation between the amount of calcium given
  and the degree of inhibition of iron absorption differs from other
  factors influencing iron absorption.
  This dose-effect pitfall is illustrated by 2 studies...[Read more in the linked article ].

A review of studies, PubMed, 2010

  The quantitative effect, although dose dependent, was modified by the
  form in which Ca was administered and by other dietary constituents
  (such as phosphate, phytate and ascorbic acid) known to affect Fe
  bioavailability. The results of most multiple-meal human studies
  suggest that Ca supplementation will have only a small effect on Fe
  absorption unless habitual Ca consumption is very low.

A study, PubMed, 1991

  When taken without food, calcium carbonate did not inhibit the
  absorption of ferrous sulphate with doses of either 300 mg Ca and 37
  mg Fe or 600 mg Ca and 18 mg Fe. However, at the latter levels,
  calcium citrate and calcium phosphate reduced iron absorption
  significantly by 49% and 62%, respectively. All calcium supplements
  inhibited absorption of the iron supplement when taken with food. The
  absorption of dietary nonheme iron was also inhibited by all three
  supplements. This inhibition was less pronounced from a meal of high
  iron availability and low calcium content (28%) than from a breakfast
  meal of low iron availability and high calcium content (55%).

A study, American Journal of Clinical Nutrition, 2005

  Calcium supplementation reduced heme and total iron without
  significantly affecting nonheme-iron absorption, regardless of meal
  bioavailability.


I think the answer is no.

The definition of polarity is basically that a molecule has a dipole, and as water has a very large dipole, if a molecule will mix with water readily, its usually pretty polar.

Water also can share its hydrogens in hydrogen bonding, which is an actual shared covalent bond where a hydrogen atom is shared between two acceptors.  The hydrogen bond is fairly weak (~ 0.5 kcal/mol) but water does a lot of hydrogen bonding.

So hydrogen bonding and polarity are often a shared characteristic of an molecule, but are not the same thing.

Ions are quite hydrophilic but do not need to be hydrogen bond donors or acceptors.   Chloride  (Cl - ) is not a hydrogen bonding atom - its so acidic that it exists nearly entirely in the Cl- form in water solution. But its definitely electro negative and really soluable in water. Are Ions polar though?  Chloride is symmetrical and so its not really polar.

Still is there a polar molecule which is neither a hydrogen bond donor or acceptor?  Acetone and the cyanide ion (CN-) are a polar molecules which have no hydrogen bond donor, but can accept them.

I think sulfate is an example of a polar molecule which does not form hydrogen bonds.
Sulfate (SO4 -- )  has four S-O bonds arranged in a tetrahedron but each of them is highly polar - with 90% of the negative charge on the oxygen.  But like the Chloride ion its so acidic that it much prefers its free ionic state.  It would have very little hydrogen bonding character even when its in water.  Sulfate can form hydrogen bonds, but I think they will only be stable when there are several of them at once.  Sulfate binding protein has seven hydrogen bonds when it binds sulfate, using the chelation effect to make the binding strong enough to be stable.


Can someone help me interpret these charts on fluorescent polarization?

These charts are flow cytometry graphs, something not explicitly stated in the figure description, but obvious to everyone who has seen similar graphs before (and I assume it's at least mentioned in the method section of the paper, I didn't read that though).

Each dot in a flow cytometry graph represents a single cell and, as you correctly identified, the PE & FITC flourescence corresponds to fentanyl and the respective proteins of interest. (The labelling was done somewhat indirectly and as is typical for flow cytometry with antibodies but that doesn't matter for the interpretation.). The dots are coloured according to their density: blue indicates only single dots and warmer colors show increased number of overlapping dots (with red being the highest).
It is also important to note that all the axes in these graphs have logarithmic scales, so the shifts you see in the graph represent shifts in orders of magnitude.

The combination of the logarithmic scale with per cell data points means, that you also see 'negative cells' on each axis: along the FITC axis (which represents expression of the protein) you can make out two groups of points. The lower one of these groups has cells that don't express the protein (meaning the florescence detected is just background from staining), while the higher groups contains cells that do express the protein (the staining for the protein is significantly above background).

If you now compare the two proteins you can see that high (protein expressing) group for Fen49 also has an increased signal for PE (which represents fentanyl), meaning that these cells bind fentanyl. In contrast with that for 2QZ3 the fentanyl signal is independent of whether the cells have a low signal or high signal for protein expression.

The bar graph on the right gives the average PE (fentanyl) levels for other additional protein variants. The figure description doesn't explicitly say whether this is the average of all cells or only the ones expressing the corresponding protein at above background levels.


How many residues can a reliable ab initio structural model contain?

Year on year reliable ab initio predictions are becoming more common for longer proteins. 400 residues is not an unfeasible length. Of course, loops still remain more of a challenge than helical and sheet secondary structures.

At CASP13, the Google DeepMind team used AlphaFold to produce a good quality model (T0594) of a 774 residue protein which is a WD40-repeat of RFWD3 (6CVZ).
All of their CASP13 entries are here.


Does the composition of a meal play a big, or small, role in food's thermogenic effect on the body?

According to Diet Induced Thermogenesis (Nutrition & Metabolism, 2004), the percent of calories converted to heat depends on a nutrient:

Proteins: 15-30%
Alcohol: 10-30%
Carbohydrates: 5-10%
Fats: 1-3%
A mixed meal: ~10% (this is an estimated average)

The thermic effect of nutrients is not a fixed value and can vary greatly within a person and from person to person:

  Reported intra-individual variability in DIT, determined with
  ventilated-hood systems, is 6 to 30% [7,8]. Reported within-subject
  variability in DIT, determined with a respiration chamber, is 43 to
  48%.


What is the heritability of brain gyrification?

Short Answer:

Genetically identical individuals do not have identical brain structure.

Longer Answer:

The easiest way to answer your question is to look at "natural" clones: monozygotic (i.e. "identical") twins.

Brain morphology is of a lot of interest in neuroscience because differences in brain morphology are often confounding factors in human brain studies (for example those using MRI/fMRI).

I'll refer to a study by White et al., 2002. They studied volumetric and surface morphology measures in monozygotic twins. They found remarkably strong correlations in total volume (r values of .98-.99 for measures like total brain volume, cerebrum volume, cerebral gray matter/white matter, and cerebellum), and still strong correlations with different lobes of the cerebral cortex (r values from .69 to .97 for frontal/parietal/temporal/occipital gray and white matter).

However, surface measures: surface area, gyral and sulcal curvature, and surface complexity were more weakly correlated (r values of 0.49 to 0.69).

Of course, because these are monozygotic twins raised together, it's hard to know how much of the similarities are due to the shared environment as well as shared genetics. However, it is clear that brains of identical twins are not identical, and in particular their brains seem to differ more on measures of cortical surface structure rather than overall brain size. The authors write:

  Many different types of nongenetic influences may contribute to the plasticity of the cortical surface characteristics, such as educational experiences, physical activity or social interactions. Furthermore, probabilistic events during the complex process of neurodevelopment [e.g. connections between neurons (Muller et al., 1997)], differences in gene expression either by chance or modulated by early-immediate genes (Abraham et al., 1993; Worley et al., 1993), or variability in cell–cell interactions (Fletcher et al., 1991) may also contribute to variability between MZ twins.

References

White, T., Andreasen, N. C., & Nopoulos, P. (2002). Brain volumes and surface morphology in monozygotic twins. Cerebral cortex, 12(5), 486-493.


That's a Western Black Widow subadult female.  The banded legs, with dark 'knees' and lighter brown intervals, become all black as the spider matures, just as the bands on the body disappear as it becomes all black.

Below is a slightly older one, where the center stripe is beginning to turn red.
Your first clue is the irregular web, characteristic of the Theridiid cobweb spiders.  The second clue is the robust body and legs, with especially long first and last pairs.  The key field mark, if you had seen the underside, is the red or orange hourglass.  It is clearly not any kind of orbweaver, simply from the web; and none of the several sorts of Argiope look anything like this spider.

Be aware that this spider can give quite a potent bite (although they often don't, preferring to hide, and not biting unless endangered).  Like the other Black Widows, they are best not handled, just in case.

https://bugguide.net/node/view/1458045/bgimage


Isolating gene of interest from a large strand of DNA

Assuming that you know exactly where in the full DNA strand the gene of interest is located, it is fairly easy to isolate the gene. There are several restriction enzymes you can use, it's just a matter of determining which one(s) are most appropriate for your gene of interest.
Remember that it is usually fine to have extra nucleotides on either end of the gene; the ribosomes will start and stop adding peptides based on start and stop codons, independent of how far the ribosome moves before reaching the start codon. Analyze your DNA strand and try to find a restriction enzyme that will slice the strand somewhere before the gene begins, and usually another that will slice it somewhere after it ends, although sometimes the same enzyme will work for both ends of the gene.
Edit: As @Untitpoi mentioned, if the restriction enzyme's slice sequence is found within the gene of interest, it will cut your gene in two (or more). It is very important to ensure that the enzyme(s)s you choose do not slice the gene of interest, otherwise the strand will be useless. It's possible to re-join the strands (which, thanks to sticky ends, isn't too difficult), but why take the extra effort when you don't have to?


Understanding Hodgkin-Huxley's model and activation variables

1) In practice, no one attempts to obtain explicit solutions for m(t), especially considering the presence of many other ion channel species, nor is there any need to. The standard of art is to use numerical simulations with a sampling interval dT that is sufficiently smaller than any relevant time constants.

2) I'm not sure what intuitive and sensible interpretation you are looking for; it may not make sense to come up with an intuitive explanation for each and every subset of terms. The use of time constants implies that the system is modeled as a linear time invariant system at a given voltage.

  What does the time constant τ(V) and its dependence on V mean? In which respect and by which hypothesised mechanism is the gate "faster", when τ is smaller?

The time constant is a scalar that describes the rate at which the system approaches some equilibrium. You could think of the changes in channel state as chemical reactions of the form:

Open <=> Closed

which has some equilibrium and some rate constant - both the rate constant and equilibrium conditions can be a function of voltage, as depicted in the figure you provide. The physical meaning of a rate constant being voltage dependent would be that the activation energy for the transition between states is a function of voltage; when the activation energy is lower, the reaction can progress more quickly (in either direction).

  How can the voltage-sensitive steady-state activation function m∞(V) be intuitively explained other than by "giving the asymptotic value of mm when the potential V is fixed (voltage-clamp)" or by some complicated description of experiments to determine it?

That's exactly what it means, and the descriptions are not complicated: the steady state value for a reversible reaction is the point at which the number of units moving from open to closed would be the same as the number moving from closed to open, so on average you see no more change: that's what steady-state means.

  What does m∞(V)−m mean, i.e. "the deviation of the current activation from the steady-state activation"?

Yes, "the deviation of the current activation from the steady-state activation" is accurate. The equation is an equation for the change of m, and the change of m is proportional to the "distance from equilibrium" - this is a characteristic of any process that follows linear time invariant dynamics. Note that there are other ways to write this equation that involve a "forward rate", a "backward rate", and the concentration of units in each state (the Wikipedia Hodgkin-Huxley page you linked has these equations), but you can simplify these to the equation you show here because some proportion of the "forward rate" process is cancelled by the "backward rate": your equation is sufficient to describe the net change.


What is the least costly method to generate sequential amino acid deletions?

Deletions may make sense if you are analyzing the N-terminus or C-terminus of a protein. If you are looking at an internal region however, keep in mind that the more AAs you delete, the more likely you are to disrupt the overall protein structure. If you delete any random selection of 8 AAs within a protein, there's a chance you'll knock out activity by changing the protein fold or stability. That's not useful information.

This question is usually first addressed by alanine scanning - sequentially or additively changing amino acids to alanine. This is much more informative than deletions. Even better, you can choose to replace wild-type AAs with other AAs of similar size but differing charge or hydrophobicity. Then you are most likely to change the function of a region without changing the structure.

The quickchange kit works great, but if cost is an issue you can do whole plasmid mutagenesis PCR with your own reagents. And make your own competent cells.

In my experience though, whole plasmid PCR can be tricky - if it doesn't work the first time it can be difficult to troubleshoot. If time is an issue, I'd recommend doing overlap extension PCR with the same mutagenic primers, plus one set of amplification primers at the 5' and 3' end of your gene. Make a large batch of digested vector, test as a negative control, and use it for ligation of all of your different inserts.


PBS or TBS, where cannot use each buffers?

I think you answered your own question.

The buffer used in a given experiment depends on the requirements and limitations of the experiment itself. You just have to look at the properties of the buffer, and if it is relevant to your experiment.

You just gave two great examples... are you just looking for more examples of experiments when one would not use phosphate buffer vs Tris buffer?

PBS is supposed to closely mimic/represent the osmolarity of a cell, and buffer from pH = 7.0 to 9.0. Tris also buffers around neutral pH. It is pretty cheap, but as you've stated, has primary amine groups that are nucleophilic and thus interfere with certain experiments like disuccinimidyl suberate crosslinking, etc.


What is it called when an animal only has one type/variation of dentition?

Homodont

You can find the term "homodont" used in Lambert et al. (2014) or on wikipedia > dentition for examples. The opposite of homodont is heterodont (wikipedia > heterodont). In mammals, a classical example of homodonts is the dolphin.


Yes, you can find mutations in the genomic DNA which affect splice acceptor sites. Wikipedia lists the following outcome:

Mutation of a splice site resulting in loss of function of that site.
Results in exposure of a premature stop codon, loss of an exon, or
inclusion of an intron.
Mutation of a splice site reducing specificity. May result in
variation in the splice location, causing insertion or deletion of
amino acids, or most likely, a disruption of the reading frame.
Displacement of a splice site, leading to inclusion or exclusion of
more RNA than expected, resulting in longer or shorter exons.

The article lists two interesting papers:

Lim KH, Ferraris L, Filloux ME, Raphael BJ, Fairbrother WG (2011). "Using positional distribution to identify splicing elements and predict pre-mRNA processing defects in human genes". Proc. Natl. Acad. Sci. U.S.A. 108 (27) 11093–11098.

Ward AJ, Cooper TA (2010). "The pathobiology of splicing". J. Pathol. 220 (2) 152–163.

Both papers are open access.


The 2nd polar body contains almost no cytoplasm, so if only this body is fertilized it contains no maternal genes to guide the development and moreover not enough nutrients. So this wouldn't work. "Source"
Moreover, there wasn't reported even any case of "twin" resulting from the fertilization of 2nd polar body according to this article

There was reported case of twins formed by a mass of fertilized ovum and fertilized (diploid) first polar body. Source

What could happen is that if both polar body and oocyte are fertilized, these two cells merge and form tetraploid embryo. Which is sometimes able to form fetus (sometimes just ends as mola hydatinosa), but definitely not able to produce a viable child in humans.


Reason behind colour of hibiscus and sunflower

Flower color is result of reflection of light due to various color pigments. Evolutionary such pigments were selected due to various reasons like to attract pollinators (Dyer et al 2012). There are two major types of flowers pigments

Carotenoids (produces yellow, orange and red colors)
Flavonoids (produces red, purple, magenta and blue colors)

However, flower color is affected by various other factors (e.g. other pigments, metal ions and its chemistry etc.) along with above pigments.

Hibiscus' dark red color is outcome of Anthocyanins which is water soluble flavonid (Grajeda-Iglesias C et al 2016). However, this pigment is highly unstable and depending on pH of the surrounding it can be red, purple, blue or black. (More details in this book). Hibiscus contains majorly delphinidin-3-O-sambubioside (Dp-samb) and cyanidin-3-O-sambubioside (Cy-samb) as the major anthocyanins (DU and Francis 1973). Chemical reaction responsible for generation and utilisation of these pigment is shown below (borrowed from Grajeda-Iglesias C et al 2016)

In above image, at low pH values $AH^+$ produces red color while  and $(A)$ produces purple/blue, which is thermodynamically unstable. In addition to that co-pigments like Hydroxylatedbenzoic and cinnamic acids, hydroxyflavones (which all are colorless) are also responsible for not only stabilizing these chemical products but enhances the color (Grajeda-Iglesias C et al 2016).


Why are the neurites from hair cells to spiral ganglion cells called axons?

I believe to understand now, thanks to @AliceD's answer to this question:

Why are Merkel cells innervated by an axon, and not a dendrite?

The axon seemingly emanating from the cell (hair or Merkel) is just by coincidence not a physiological part of the cell (hair or Merkel), but its functional axon. The tactile meniscus (in the case of the Merkel cell) plays the role of an "out-sourced" axon hillock of the cell (hair or Merkel) which possesses no axon hillock (and axon) on its own.