In the NCBI Taxonomy tree what does "no rank" mean?

Well, welcome to Phylogenetic Systematics.

The Linnaean Taxonomy is a rank-based classification system. When Linnaeus first proposed it in 1735, in his famous Systema Naturae, he created 5 ranks: Regnum, Classis, Ordo, Genus and Species (in Latin).

Today (more on that below) Linnean Taxonomy uses 8 main ranks:

Domain
Kingdom
Phylum
Class
Order
Family
Genus
Species

If you add the prefixes super-, sub- and infra- to that, you get more ranks.

However, in the 60's, a new systematics was proposed by Hennig, called Phylogenetic Systematics. I'll not explain in details what Phylogenetic Systematics is in this answer, there are plenty of good sources for you to read about. My point here is only one: showing you that there is no rank in Phylogenetic Systematics.

Have a look at this cladogram:

The group made by A + B is a monophyletic group. The group made by A + B + C + D is also a monophyletic group. The same way, the group made by A + B + C + D + E + F + G + H is a monophyletic group (by the way, there are 7 monophyletic groups in that cladogram). And all those groups have names.

Now comes the important part: in Phylogenetic Systematics, the number of monophyletic groups between the more exclusive set (you) and the more inclusive set (your very first ancestor, more than 3 billion years ago) is enormous! It is, of course, way bigger than 8 (or than 32, if you add all those prefixes). Even if you add uncommon ranks, as Tribe  or Section, you don't get even close to the number of monophyletic groups between you and your oldest ancestor.

As I read some time ago in a phylogenetic systematics paper: "We need names. Lots of names!".

That's why modern taxonomy has a problem with the traditional notion of ranks, some biologists defending that we should drop the ranks altogether (except, of course, the Species). And that's why I was uncomfortable in writing today some paragraphs above: there is an increasingly number of biologists that use phylogenetic nomenclature, which is incompatible with Linnaean taxonomy.

So, to give you an example: Mammalia is a Class. However, Mammalia lies inside a higher group, that we call Synapsida. Synapsida is neither a Class nor an Order nor a Phylum... it does not have a rank. Synapsida, by its turn, lies inside Amniota (animals with amnion), which also doesn't have a rank...

The examples abound: Sauropsida, Eudycots, Opisthokonta, Reptiliomorpha, Viridiplantae etc are all groups without a rank.

Thus, when a biologist says "that organism is an Amniota", she/he is just saying that the given organism belongs to the monophyletic group called Amniota. If you ask him/her "what is Amniota? A Class, an Order, a Superfamily, a Subphylum?", the answer will be: "none of them". Monophyletic groups don't need to have a rank in Phylogenetic Systematics.

Finally, quoting the Taxonomy Help from NCBI:

  The ‘preferred scientific name’ for a taxon may be either formal (e.g. Homo sapiens) or informal (e.g. Homo sp. Altai, or uncultured fungus). Taxa above the species level may also be either formal (e.g. the order Mammalia) or informal (e.g. the unranked node eudicotyledons). (Emphasis mine)

Source: https://www.ncbi.nlm.nih.gov/books/NBK53758/#taxonomyqs.Overview


Why do cell membranes have a lipid bilayer instead of a monolayer?

Why use membranes?
Compartmentalising the cell has lots of advantages and purposes. In Koshland's 2002 essay, compartmentalisation was described as one of the seven fundamental pillars of life. Broadly speaking, membranes create different sets of conditions (chemical and biological) inside the cells. This allows more efficient functioning and advanced catabolic and metabolic processing. More complex and adaptable systems were thusly achieved by the evolutionary process.
Why a bi-layer?
There have been several molecular dynamic simulations such as this one carried out to investigate the biophysicochemistry of spontaneous bilayer assembly. There, lipids start in random orientations. The ordered bilayers we know and love spontaneously assemble in under 100ns. What's actually happening at a molecular dynamics level is the self-association of the hydrophobic lipid tail groups driven entropically by water. In other words the polar (hydrophilic) head-groups "prefer" interacting with the water (called the interfacial region) and the the hydrophobic tail groups "prefer" not interacting with the water. With those two preferences in play, the lipid bilayer forms.

On a smaller scale, micelles also form spontaneously, but this doesn't offer the compartmentalization required for biological functions.

It would appear that the conditions for an ordered bilayer are so favorable that they take precedence over any other orientation or combination. One apparent exception is the archael monolayer. Do see @WYSIWYG's answer that refers to the exceptional extremophiles that use a monolayer. Their comment summarises the monolayer succinctly:

They are technically monolayer but resemble bilayer. Like bilayer connected via a covalent bond. These membrane lipids have two hydrophilic heads and a hydrophobic "torso".

Image sources

Image 1: http://www.perkepi.com/cell-membrane/
Image 2: https://en.wikipedia.org/wiki/Lipid_bilayer


About the apoptosis mechanisms in a cell

Not at all. In order to self destruct, you don't need to disable all necessary functions, you just need to disable one. That's why the functions are called "essential". To take a very simple example, in every movie you've seen where the self destruct has been activated, that self destruct mechanism was almost certainly a bomb that blew the ship/installation/planet or whatever up. The self destruct did not go around disabling individual processes, it just activated a bomb and destroyed everything.

Apoptosis is quite similar. While there are many essential processes in a cell whose failure can activate apoptosis, the mechanism of apoptosis itself usually involves the straightforward destruction (lysis) of the cell. Simply put, the cell digests itself, breaking down its various constituent parts and, finally, destroying the cell membrane and breaking up the cell itself. For a summary see this Wikipedia page or here.

Briefly, when apoptosis is triggered, the caspase cascade is initialized which results in the breakdown of various proteins in the cell and, finally, in cell lysis. It really is analogous to setting of the bomb that destroys the facility of the bad guys.


Why do bumble bees run repeatedly into walls?

Crall et al., 2015, studied bumblebee collision avoidance (note the senior authors are the same from your link). It seems that, contrary to popular belief and experience, bumblebees are actually quite good at avoiding collisions, but they are also in an environment that has a lot of obstacles, so collisions still happen frequently.

There is a lot of interesting content in that paper, but one of the interesting discussions was about types of collision avoidance by body size. The authors note that for larger animals, collision avoidance strategies tend toward reversal/slowing down to reduce impact, whereas in smaller animals, strategies tend toward direction-change. This might be because collisions at high speeds are more dangerous for larger animals, so slowing down is the priority. Accelerating in a lateral or vertical direction, instead, would result in a full-force collision if the acceleration was insufficient to avoid the object (I have to admit, though, your gif doesn't seem to show any deceleration).

Larger individuals in their study performed more slowly on their obstacle course than smaller ones, but it seemed like all the bees were pretty good at avoiding obstacles.

Based on this study, I don't know that we can conclude definitively why bumblebees repeatedly run into walls, but given how well they navigate an obstacle course like this I am guessing it isn't simply because they are incapable, but rather has to do with a few things:

Walls are somewhat unexpected obstacles; bumble bees are probably best evolved for navigating around foliage that has a limited horizontal size, and once headed home they are expecting a direct route to be most efficient. A good transit strategy in that case would be to fly slightly laterally in the event of a collision to find a new opening, but not deviate too much from the original path of travel.
Speed/collision tradeoff. Getting home fast can have some obvious advantages because it increases the effective foraging potential. If collisions can be mitigated or aren't damaging, it might make sense to fly at high speed and just deal with the collisions as they come.
Bumblebees are big. Therefore, it's harder for them to stop, and they might use a strategy for collision avoidance that reduces impacts rather than avoids impacts altogether.
Cognitive biases in humans. Bumblebees make quite the racket when they run into things. You're going to hear it each and every time if you are nearby. The same isn't necessarily true for other bees or other insects.

References

Crall, J. D., Ravi, S., Mountcastle, A. M., & Combes, S. A. (2015). Bumblebee flight performance in cluttered environments: effects of obstacle orientation, body size and acceleration. Journal of Experimental Biology, 218(17), 2728-2737.


Are epigenetic modifications the most stable mechanisms for cell differentiation?

Epigenetic marks are reversible (you might be aware of induced pluripotent cells). Many animals can regenerate organs with high tissue complexity (such as a limb) and this involves de-differentiation in some species (Sandoval-Guzman et al., 2014). Even otherwise, cells can respond to extracellular/environmental cues to modify their epigenetic state (for e.g. EMT involved in wound healing). I would still consider epigenetic marks to be more "stable" than simple regulatory mechanisms.

Only way for a cell's identity to actually become 'locked in' is by genetic changes. The maturation of lymphocytes (especially the B-cells), would be a good example. These genetic changes happen via V(D)J recombination, class-switching recombination and somatic hypermutation.

L1 retrotransposons are also known to contribute to somatic heterogeneity in the brain neurons. However, the frequency of insertions is not very high (Evrony et al., 2012).


Are there any documented cases of extinction of a species of fungus?

According to the International Union for Conservation of Nature’s Red List there are many endangered fungi, but none that are documented to have become extinct within the time frame of interest to you.

However, it seems likely that some fungi have gone extinct with their plant hosts — according to the IUCN there have been 133 documented extinctions of plant species. In particular, mycorrhizal1 (and other) associations between plants and fungi are prevalent and some of these associations appear to be specific (i.e. the fungus only associates with one plant species). For example, there are reported to be 28 species of fungi that only associate with the shrub Lantana camara.2

References:
1: Hoeksema, J. D., Bever, J. D., Chakraborty, S., Chaudhary, V. B., Gardes, M., Gehring, C. A., ... & Lajeunesse, M. J. (2018). Evolutionary history of plant hosts and fungal symbionts predicts the strength of mycorrhizal mutualism. Communications biology, 1(1), 116.
2: Hawksworth, D. L., & Rossman, A. Y. (1997). Where are all the undescribed fungi?. Phytopathology, 87(9), 888-891.


The name is derived from the sugar which is bound to the base. For RNA it is Ribose (that why it is called ribonucleic acid) and for DNA it is Deoxyribose (hence the name deoxynucleic acid). The deoxyribose is missing an OH-group at positition 2 of the sugar ring, the name literally means "without oxygen". See the image below (from here) for further clarification:


Question a

The only possible genotype that brings a phenotype of 12 inches is: $AABBCC$. Similarly the only possible genotype that bring a phenotype of 6 inches is: $aabbcc$. In consequence the offsprings can only be: $AaBbCc$ which measure $2+1+2+1+2+1 = 9$ inches.

Question b

Now the question is: if we breed two $AaBbCc$ how many offsprings measure 11 inches? Because there are three bi-allelic genotypes you have $2^3=8$ possible gametes and therefore you have to draw a 8x8 punnett square. Doing so, just count the proportion of offsprings that measure 11 inches. You can reason slightly more logically and get a faster answer. To measure 11 inches you need to have only capital letters in your genome except at one position. In consequence, if your father gives the gamete $ABC$, you mother should give the gamete $ABc$, $AbC$ or $aBC$. You can inverse the role of the father and the mother and it works as well. Therefore, you have 6 possible combinations that give rise to an offspring that measure 11 inches. Because there are $8 \cdot 8 = 64$ possible combinations, the proportion of offspring that are 11 inch-long is $\frac{6}{64} = \frac{3}{32} = 0.09375 ≈ 0.1$. About 10% of your F2 individuals are 11 inch long.


Proteins that give color (without fluorescence)

Have a look at this paper. They have isolated a chromoprotein similar to GFP, and like the latter it does not have any prosthetic group.

This protein — asFP595 (because it was isolated from the anemone  Anemonia sulcata.), is purple coloured under white light and also exhibits a little fluorescent emission in the red region  (λmax = 595 nm).

Also have a look at these two papers:

GFP-like chromoproteins as a source of far-red fluorescent proteins
Major colour patterns of reef-building corals are due to a family of GFP-like proteins


Are carbohydrates an essential component of human diet?

From a theoretical perspective this is a very interesting question, mostly because it is difficult to completely abstain from carbohydrate intake on a normal diet. Even the popular low carb diets of the late 1990s and early 2000s (e.g. Atkins Diet, South Beach Diet) were just that, they were Low Carb, Not No Carb.

We know there are essential dietary nutrients for humans, like essential fatty acids and essential amino acids. The reason that these must be obtained in the diet is because humans do not have the enzymes to synthesize these nutrients de novo (aka, "From Scratch").

From a biochemical perspective we know that fatty acids and acetyl-CoA cannot be converted back into glucose or other carbohydrate intermediates. This is because of the irreversible biochemical reaction catalyzed by pyruvate dehydrogenase, which converts pyruvate to acetyl-CoA. Thus, fatty acids (lipids) can be oxidized to acetyl-CoA (for the TCA/Krebs Cycle) but cannot be further converted to glucose within the body.

In terms of protein, however, amino acids are either glucogenic, ketogenic, or both. If amino acids are ketogenic, then this means they can be converted into acetyl-CoA for the Krebs Cycle. If amino acids are glucogenic, then it means that they can be broken down into glucose. The breakdown of amino acids can be used to synthesize glucose or for anapleurotic reactions of the Krebs Cycle.

As stated in the editorial noted in the comments of this question (From the American Journal of Clinical Nutrition), there are daily "requirements" for carbohydrates. However, it does not appear that any diseases are unmasked by very low to zero carbohydrate absorption (which is most closely occurs in the Inuit populations whose diet is entirely fat and protein).

So, if you ask the question "are carbohydrates essential components of a human diet?" the answer would be probably not. However, as mentioned above, carbohydrates are ubiquitous and it is impossible to abstain from all carbohydrate intake.

Below is a picture freely available online from this website (from Lehninger Principles of Biochemistry, 5th Edition) of the glucogenic and ketogenic amino acids and the metabolic intermediates to which they can be converted. This is how Krebs Cycle intermediates can be generated from amino acids and are not dependent on dietary carbohydrates.


ATP yield of fermentation: study to cite?

For glycolysis this is really not so much of an issue, because the ATP yield is fixed by stoichiometry. The early biochemistry work by Embden, Meyerhof, Parnas and other that mapped out the reaction mechanisms of the glycolytic pathway shows that you always obtain exactly 2 ATP per glucose; this is simply the stoichiometry of those reactions. There are a number of primary papers documenting these reaction mechanisms, but it's a large undertaking to go through all of it; the glycolysis chapter of Stryer's Biochemistry is a good summary I think. A brief review of the historical development is described in: "A Fresh View of Glycolysis and Glucokinase Regulation: History and Current Status".

For respiration it's very different, since there is no fixed stoichiometry for chemiosmosis --- the ATP yield depends on the proton gradient across the inner mitochondrial membrane, which in turn depends on a number of factors. So in this case ATP yield will differ between cell types and conditions, and must be measured experimentally.


Are 2A cleavage sites functional in bacteria?

2A self cleaving peptides do apparently work in bacteria (as the papers in your question suggest), but it seems that they are not commonly used in these chassis simply because they are not needed.
For context, in prokaryotes, translation is initiated by the ribosome binding to a shine-dalgarno (SD) sequence on the mRNA. These SDs can be placed anywhere along the mRNA strand, and so multiple SDs can be present. This means that translation can begin at multiple points along the mRNA, and hence proteins can be co-expressed by one promoter by including multiple RBSs and stop codons within the expression unit (i.e. promoter-RBS-CDS1-stop-RBS-CDS2-stop-terminator).
However, in many eukaryotes, translation begins at the 5' end of the mRNA where the ribosome is assembled, and scans along the mRNA until it finds the start codon. Once the protein has been synthesised and the stop codon reached, the ribosome falls off of the mRNA. This means that if there was another CDS encoded after the first stop codon, it won't be translated.
It should be noted that it is possible for eukaryotes to generate mRNA encoding multiple proteins, but as it was assumed for a long time that this was unique to prokaryotes, there is less research for this in eukaryotes. This paper has some useful information: https://academic.oup.com/femsyr/article/2/2/215/536601.
Because of these differences, for most applications, if co-expression in bacteria is required it is much simpler to add in multiple RBSs and stop codons than to rely on something like 2A peptides which, as you mentioned, do not always work and can result in fused proteins. However in eukaryotes, techniques such as 2A peptides are important considerations for co-expression as poly-cistronic mRNA (mRNA encoding multiple proteins) seem to be much less common.
This doesn't mean that there aren't applications for 2A peptides in bacteria, but they are much more specific and hence their use doesn't turn up so much in the literature.
These wikipedia pages have some good reading and references:

https://en.wikipedia.org/wiki/Internal_ribosome_entry_site
https://en.wikipedia.org/wiki/Eukaryotic_translation

Disclaimer: I don't work with eukaryotes so most of the information about gene co-expression and how common it is has been gathered from reading for this question.


Breathing becomes harder in certain wind conditions

So I'm going to go ahead and tell you outright that it is not the diving reflex.

What you are experiencing is the effect of air pressure.

Our lungs work off of pressure. Specifically our lungs inflate by using "negative pressure" (a word I've always hated). The pressure is not actually negative it is simply lower than the surroundings. Since there is less air in your lungs the air from the atmosphere rushes in because the pressure is higher outside your lungs. This is Boyle's Law (not the pressure outside being higher, but what happens when your lungs expand). Where an increase in Volume means a decrease in Pressure (if all else remains unchanged). In fact plants pull water up using negative pressure.

However to push out the air from our lungs we supply pressure using our muscles that overcomes the outside pressure and forces the air out.

The reason you feel your breathing change is because when that train passes by you correctly observed the strong gust of wind. This gust of wind has some force behind it that normally is not in the air you are breathing from the atmosphere. It has more force which increases the air's velocity. This actually decreases the pressure, but there's no need to get into that here (Bernoulli's).

The reason it feels like your body is "fighting to breath" is because the air is traveling in a direction with some force that you need to overcome by opening up your lungs just enough to "suck" the air in with negative pressure. This is more than the pressure you usually need to produce in order to breath in air that is "still".

What is funny to think about is we don't really have a muscle that "pulls" air in, even though it feels like you are actively doing that. The air actually rushes in on its own. All you do is expand your rib cage, which your lungs are attached to (look up on how, it's actually pretty cool), thereby making inhalation occur.

Now an interesting question for you to ask yourself is why is cold air harder to breathe?


What happens when the conductance of a sodium channel increases?

No, not quite. You are on the right lines, but incorrect in thinking that intracellular sodium concentration is higher.

At the resting phase of a neuron, there is less sodium inside the cell and more sodium outside the cell. An ATPase sodium potassium pump is constantly pumping 3 sodium ions outside the cell for every 2 potassium cells that enter the cell.

For voltage gated sodium channels to open, there must be a significant change in voltage, which can be triggered by the binding of neurotransmitter to receptors for example. This triggers the sodium channels open and sodium will flood into the cell due to a high concentration gradient (because there are more sodium outside than inside) but also due to an electrical gradient (the neuron is more negative on the inside; positive sodium ions will be attracted to the inside).

Because sodium is flooding into the cell, this will cause the membrane potential to become more positive (depolarised) and will eventually reach an action potential (30mV). After an action potential, the channels will become de-activated and shut. After a period of hyperpolarisation, the neuron will return to a resting state.

Source: https://en.wikipedia.org/wiki/Action_potential


Can someone suggest me good opencourseware links for learning computational biology basics?

http://ocw.mit.edu/courses/health-sciences-and-technology/hst-508-genomics-and-computational-biology-fall-2002/audio-lectures/

Download all the slides if you want good resources.


Difference between morphogens and evocators in development?

"Since the evocator Waddington and Needham discovered was ether soluble, it was considered to be a sterol, a class of molecules that includes many hormones related to later development" (https://embryo.asu.edu/pages/chemical-induction).

It seems like the termed is outdated, hopefully, you find this information useful.


Are Lambic beers the product of quorum sensing?

Almost certainly not. Species occupy different niches due to their differing growth rates and tolerances. Interspecies quorum sensing and the symbiotic relationship that implies do exist(see: lichen), but open-air inoculation is unlikely to produce them.

Why would the Brettanomyces simply kill time waiting for 'their turn'? It's likely they don't grow as fast as S. cervisiae or other early fermenters, and as a result they're outcompeted until alcohol content rises enough to slow or stop other species. Brettanomyces isn't 'waiting', they're eating and growing as fast as they possibly can.

Many microorganisms form spores or simply hibernate until conditions are favorable for growth. For highly acid and alcohol-tolerant species, perhaps they sporulate until the mix is acidic enough to guarantee them habitat. This is a form of quorum sensing, but the transmission medium is pH and alcohol concentration.


Short Answer

In a nutshell, DNA sequencing technology has a limit to how long a stretch of DNA it can read in one go.

Long Answer

So what most commonly occurs is the length of DNA you wish to sequence needs to be (almost randomly) chopped up into given lengths (depending on the technology) and each length or read is sequenced in parallel. But now you don't know which lengths to stick together! i.e. the ordering of these chopped up lengths. So you sequence it many times over (deeper) and this way you can align contiguous ends of these lengths together like a jigsaw puzzle. The more times you sequence the more accurately the 'contigs' will be aligned.

DNA Assembly Diagram

Comment if you want more details, but the technical term you want to google is "sequencing assembly".

Here's the wiki

:)


How do birds learn their tunes in isolation from their own species?

Birds have to learn their song patterns.
They are able to chirp, but the songs with "meaning" are learned from their parents or whatever they learned to be their "parent".

Here is a paper that related bird song learning to human learning (of speech, for example).
Birds brought up by parents from another species learned to sing their songs.
There are many birds that learn to imitate other animals or sounds, so in isolation from all birds they will probably do this.

I can't recall where, but I read a paper once, where little finches brought up by humans developed a song resembling the "Hello there, now there's food", their caretaker always greeted them with. (Not the speech, but the overall sound pattern.) They might not understand the signals, but they try to communicate nevertheless. Some birds use sound from other species to mock others, scare them off or lure them into thinking they might be more powerful than they are.

Birds brought up in total isolation do sing, but not the typical songs you know from their species. Deaf birds who can't hear themselves, though, do not (always) sing.


Short answer:

Nitrogen fixation (i.e, atmospheric nitrogen)

Longer answer:

Nitrogen fixation is the process by which atmospheric nitrogen is converted to forms usable by further biochemical reactions. Some bacteria are capable of nitrogen fixation (and some plants have symbiotic relationships with nitrogen-fixing bacteria); all the others rely on those species directly or indirectly to provide nitrogen.

The microorganisms involve in brewing kombucha tea are actually a collection of different species of bacteria and yeast. The bacteria that are found in kombucha tea include Acetobacter nitrogenifigens and Gluconacetobacter kombuchae, both of which are capable of nitrogen-fixation (and there may be others).

Molasses is also often used as the sugar source for kombucha, and molasses includes some nitrogen-containing compounds.

See the following review for more information:

Jayabalan, R., Malbaša, R. V., Lončar, E. S., Vitas, J. S., & Sathishkumar, M. (2014). A review on kombucha tea—microbiology, composition, fermentation, beneficial effects, toxicity, and tea fungus. Comprehensive Reviews in Food Science and Food Safety, 13(4), 538-550.


The first quote is correct. 'Microsome' is more of a lab term. This is because, as said they are found (re-formed) after centrifugation and as such aren't seen in an intact cell. Differential centrifugation is a technique used to separate cellular constituents into fractions. To quote,

  The microsomal fraction is the pellet produced when the postmitochondrial supernatant is centrifuged at 50,000g for 60 minutes. Microsomes are small vesicles enclosed by a biological membrane. During centrifugation, the endoplasmic reticulum is fragmented into microsomes

The microsomal fraction may also contain pieces from the plasma membranes apart from those from the ER.


Best colour for a dog to track an object against green background

Dogs are a dichromatic species, featuring only a long wavelength (L) and a short wavelength (S) cone (source: Smithsonian). As such, they are thought to perceive mainly blues and yellowish hues (Fig. 1). This is unlike trichromatic species like humans, who are able to distinguish red and greens as well (Fig. 2). Whether dogs perceive greens or yellows is hard to say, but either way, they see those longer wavelengths (red, green, yellow) as one hue (say, yellowish).

Hence, in dogs, green hues are basically seen as yellow (or vice versa) and indeed blue (short wavelengths) are best to create a good color contrast.

Of course, brightness contrast will work fine too (white and black).

Fig.1. Dichromatic (dog) color spectrum. source: Dog Vision

Fig. 2. Trichromatic (human) color spectrum. source: Dog Vision


What is the functional and structural distinction between core (H2A, H2B, H3,H4) and linker(H1/H5) histones?

The core histones are H2A, H2B, H3, and H4, and the linker histones are H1 and H5. The structure of the nucleosome is well explained in wikipedia:

  Two of each of the core histones assemble to form one octameric nucleosome core particle, and 147 base pairs of DNA wrap around this core particle 1.65 times in a left-handed super-helical turn. The linker histone H1 binds the nucleosome and the entry and exit sites of the DNA, thus locking the DNA into place and allowing the formation of higher order structure. The most basic such formation is the 10 nm fiber or beads on a string conformation. This involves the wrapping of DNA around nucleosomes with approximately 50 base pairs of DNA separating each pair of nucleosomes (also referred to as linker DNA). The assembled histones and DNA is called chromatin. Higher-order structures include the 30 nm fiber (forming an irregular zigzag) and 100 nm fiber, these being the structures found in normal cells. During mitosis and meiosis, the condensed chromosomes are assembled through interactions between nucleosomes and other regulatory proteins.

The core histones have a positive net charge, which facilitates the interaction with the negatively charged phosphate groups of DNA.

Apart from defining the nucleosome structure, the function of the core histones is regulatory: it can switch on/off gene expression by histone modifications like acetylation or methylation.

The gene expression is ON when there is:

• DNA demethylation

• histones acetylation
• H3K4 methylation
• H3K36 methylation

• H3K9 demethylation
• H3K27 demethylation

The gene expression is OFF when there is:

• DNA methylation
• histones deacetylation
• H3K4 demethylation
• H3K36 demethylation
• H3K9 methylation
• H3K27 methylation

// H3K4 demethylation is abbreviation for: Lysine 4 of H3 is demethylated.

Berger SL. 2002. Histone modifications in transcriptional regulation. Current Opinion in Genetics & Development 12: 142–148 is also a nice review.


Plant's phylogeny tree to identify which of them are closer (genetically) with another plant

In general for plants, before you start trying to make your own phylogeny, you should try to find an existing phylogeny. Phylogenetics is complex, and a lot of people have already done the hard work. You can start by looking at the Angiosperm Phylogeny to figure out which species are most closely related. To make use of the tree you will usually have to look up each species to figure out what order or family it is in.

In this particular case, Sorghum bicolor is a grass, so of course it's going to be closed to Zea, Oryza, Setaria and Brachypodium (all grasses) than any of the others. You can see where it places relative to the other grasses by looking at a grass-specific phylogeny. Because all three are model species, their phylogenetic placement relative to one another is well established. A simple Google image search for [grass model species phylogeny] gives you your answer (from the Setaria genome paper):

This shows you that Sorghum is closest to Zea out of the species you listed.


Is it possible for human body to convert carbohydrates to protein?

Essential amino acids cannot be synthesized from carbs, but non-essential amino acids can be synthesized. Intermediates from the citric acid cycle or pyruvate can be used to synthesize at least 11 kinds of non-essential amino acids. They will be incorporated into muscle, but you need all the essential amino acids available in order to produce complete proteins that will build muscle tissue. Proteins are made from the entire repertoire of amino acids, and I don't think there exist any (perhaps very, very few, none to my knowledge, *I've checked the literature) that are made from only non-essential acids.


What equation to compare protein isoforms in a Western Blot?

In my opinion you should use this formula:

$$ \frac{\text{log}_2(\text{Iso}_1/\text{Iso}_2)}{\text{log}_2(\text{GAPDH})} $$

This will normalize the relative fold differences between the isoforms with the loading control- GAPDH.

Since both numerator and denominator are log transformed they are in comparable domains unlike the formula-2 that you mention in your question. This is just a modified formula-2.


IP3 is indeed degraded, this is done by a specific phosphatase which is called "Phosphoinositide 5-phosphatase (INPP5A)". It catalyzes the reaction in the following way:
1-phosphatidyl-1D-myo-inositol 4,5-bisphosphate + H2O $⇌$ 1-phosphatidyl-1D-myo-inositol 4-phosphate + phosphate
The enzyme cuts of the 5'-Phosphate group and leaves 1,4-Inositolphosphate, which is subsequently recycled. The schematics looks like this in the left side (figure 1 from the reference):

Reference:
Inositol trisphosphate 3-kinases: focus on immune and neuronal signaling


What is the close and related genome used for in Gene models?

Why a related genome helps:

1) Alignment of the reads first and assemble next.
 2) The gene-space is already predefined ( the genes and their co-ordinates are already known), so if your assembly is fragmented or missing a portion of the gene information, that can be accomodated with reference genome.

Limitations: Rather than assembling your own genome, you are forcing the reference genome to be part of your genome assembly. If at all, any differences are there, they are washed out, when you do a reference assembly.


Why are the other bases not used for RNA capping and tailing?

I don't think definite answers exist but I can think of theoretical reasons:

First, Poly A tail can efficiently be synthesized because ATP is the
most readily available nTP, being the main energy source.

More to the mechanism, but this is no explanation to the evolution:
The termination sequence 'TTTATT' on the DNA template and 'AAUAAA'on the RNA is the start of poly-adenylation. But this falls in the 'chicken-egg problem' category.

As a bioinformatician, I happen to know, that 3'UTR is highest in A-content of the 3 genomic contexts and the 5'UTR is highest in G-content of the 3 contexts, so possibly these post-transcriptional modifications further strengthen the compositional differences of the contexts.

For the poly-A tail it might also be relevant to mention that G or C sequences have higher propensities towards structure due to amount of hydrogen-bonds.

I hope there were some helpful pieces of information.


How to define "Quasifixation" in continuous approximation of finite population?

As I haven't found any guideline, I just went with chosing a threshold at $p = 1-\frac{1}{4N}$ for a diploid population. Allele $A$ is therefore considered quasifixed if its frequency $p$ is greater than $1-\frac{1}{4N}$ i.e. the number of occurrences (count) or the other allele is lower than $\frac{1}{2}$.


Why do denatured proteins tend to be less soluble than the native protein?

Background information

A native protein has it's hydrophobic amino acids folded inwards, so it has a hydrophobic core. why? Because it's thermodynamically favoured. When a protein is denatured the hydrophobic amino acids won't be longer inside the core of the protein, but instead will be exposed to the hydrophilic environment (assuming you are talking about a protein inside an organism). But this isn't thermodynamically favoured because hydrophobic parts cannot form H-bonds with water and so aren't much soluble in water:

So when this happens, many protein molecules will aggregate like soap micelles (because hydrophobic interactions are favored). This will lower the total surface area of hydrophobic amino acids in contact with the water, thus lower disturbance in H-bonding in water molecules.

Here's my self-made depiction of effect of organics molecule on H-bonding in water (its quite rough, so don't care about fine details).

Summarized
hydrophobic amino acids will be exposed to the hydrophilic environment --> the proteins will aggregate together --> insoluble plaque.


Do all sea creatures that have scales have to have fins?

How about marine reptiles? Sea snakes have a paddle-like tail, so perhaps you would claim that as a fin, but maybe marine iguanas would qualify? And, of course, sea turtles.


Does avocado and orange have a common ancestor?

Here is a website that presents very accuerately the tree of life: tolweb.org/tree

Yes, they have a common ancestor just like any other living things! How closely related are they?

Both species are:

Eukaryotes (cells with a nucleus)
Archaeplastidae (plants)
Angiosperms (flowering plants)

Then, they split their way! Here is the tolweb.org page that correspond to this speciation: http://tolweb.org/Angiosperms/20646

The avocado is in the Laurales family: http://tolweb.org/Laurales/20672

The orange is in the Rutacea (sapindales, rosids, eudicots) family: http://tolweb.org/Sapindales/21051.

You can use the left arrow on the tree of these pages to come back through times and see the different speciation event that seperate both species.

While the orange is a eudicots, the avocado is part of the magnolids. The oldest fossil records of an angiosperm lived about 132MYA (see Crane et al., 2004). So the two species diverge for quite a long time! In order to give a comparison, they are as distant than humans and rabbits (it is a rough personal estimation, I don't have any reference for that!)

Note: The orange is called Citrus sinensis in latin. The species originated in China. The avocado is called Persea americana and it originated in central american (as their names indicate).

I don't know what make you feel that they are closely related. Maybe someone might say some words about their chemical compounds (and their flavour) but at first glance these two fruits taste very differently to me. Or maybe they have some remarkably similar phenotypic traits due to convergence evolution... I don't quite know about that!


I found that using the Femtotip loaders gives a continuous block of liquid, which can then be moved to the end of the tip by injecting several times. It is fine to have a air above the liquid at the tip.


Are there animals / mammals which only have one eye?

All mammals have exactly two eyes, though the eyes are vestigial in some species, some of which are even blind.

Small fossorial (burrowing) mammals generally have very tiny externally visible eyes or eyes that are covered with skin (e.g. golden moles). Some river dolphins (e.g. "blind dolphins") also have very small, vestigial eyes.

Some reptiles (and amphibians?) have a "third eye" called a parietal eye. However, it isn't a true eye. (See How Humans Lost Our Chance at a Third Eye).

I'm not aware of any vertebrates that have just one eye. As far as I know, all vertebrates have two eyes. The anableps is a fish that is nicknamed "the four-eyed fish," or something like that, though it actually has just two eyes.

However, there are one-eyed invertebrates, including copepods. (One copepod genus bears the scientific name Cyclops.) Answering your first question, copepods reportedly lack depth perception. There may be other one-eyed invertebrates, but I'm not an expert on inverts (there are too many species to count let alone study!).


Why is defibrillation in asystole ("flat line") useless?

In layman's terms: an Asystole is not affected by the electric shocks of a defibrillator. A defibrillator is used when the heart goes in fibrillations because it actually CAUSES an asystole. The idea is that you basically reset the heart to a blank state so you can start normal CPR procedure to help the heart go back to a normal rythm. That's why you see them applying CPR between shocks.

sources:

http://emedicine.medscape.com/article/757257-treatment

http://en.wikipedia.org/wiki/Defibrillation#In_popular_culture (citation needed)

http://calsprogram.org/manual/volume3/section12/CV/08-CV7AsystoleTreatment13.html


What are the best detection medias for cholera?

You should use Thiosulfate-citrate-bile salts-sucrose agar for the detection of all vibros, including cholera.  When cholera is presant, you should expect round, largish (not huge), yellow colonies.  This is the CDC recommended diagnoses method.

Again this question might be better phrased "what are the best detection medias for cholera," or "what plate screens should be conducted when vibros are suspected?"


How can the layperson test whether a UVC light sold as "germicidal" is a fake or probably the correct wavelength?

You can do the banana test to identify if it is real or fake.
Get a green banana and cover parts of it with a sticker you now need to expose the banana with the uv light for about one hour,the green banana will get brown/yellow at the exposed part and stay green under the sticker if the uv-c light is genuine..
It is best to do this in a dark room and the banana can not be in a plastic bag or any covering as this might stop the uv-c light.
The uv source needs to be close to the banana for this to work.
If the color of the green banana stay the same after the test your uv-c light is fake.
Never look directly at the uv-c light and do not shine the light on your bare skin.
source https://www.reddit.com/r/BigCliveDotCom/comments/gj9ymb/uvc_the_green_banana_test/


Why do Great White Sharks not survive in captivity?

Most of the reasons why Great Whites are hard to keep in captivity are actually quite practical in nature:

Great White Sharks are expensive to keep because they eat a lot of food; their tanks need continuous re-stocking;
They refuse to be fed by humans, leading them to die of starvation. They do not seem to accept dead small fish for food;
The correct saline balance seems very important and difficult to maintain;
Logistics are difficult; they have to be safely captured in the wild, transported to a tank and that all the while keeping them in appropriate living water;
Due to their size and aggressive nature, great whites are hard to handle;
As you said already in your post; they are open water fish and cannot be confined. Sharks can swim hundreds of kilometers within a matter of days. This exercise and freedom may be essential to their well-being. A small 4-feet 'Great' White was kept alive for 6 months in a 1-million gallon tank. And even that was hardly enough;
They seem to get depressed in captivity. Great White Sharks that are kept within tanks have been known to head butt their noses into the glass walls and lose their appetites. It has also been noted that they get increasingly aggressive in their depressed state.

Sources
- IFL Sciece
- Science Alert
- Shark Bookings


Evolution and different number of chromosoms? (a non-biologist)

Speciation doesn't happen from one generation to another, it is a slow and continuous process, and for each changing that is kept by natural selection, there are millions of changes that resulted in less functional phenotypes and were negatively selected, and another million of changes that were lethal hence soon aborted (e.g. a mutation that causes an embryo to die even before a fruit or animal can get any development). So it might be possible that many chromosome number changes are taking plane in many organisms, but they  never will estabilsh in their populations. On the other hand, some numerical changes (and all the genetic processes that follow any change) may result in a good fit, and the individuals survive, establish and reproduce. But keep in mind that it is a slow and continuous process.

Theoretically, if among Chimpanzees, multiple offsprings outcome with 46 instead of 48 chromosomes:

In a theoretical scenario: They could be able to reproduce only among themselves (the 46-chromosomed-individuals) and, with time, accumulate some differences in relation to the 48-chromosomed-Chimpanzees, and them they would be named as another species.
In a theoretical scenario: In some conditions, they might be able even to reproduce with 48-chromosomed-Chimpanzees (e.g. if this numeric change resulted from fission of one chromosome, and when the two gametes meet, the two half chromosomes of one parental pair with the whole chromosome of the other one... That is not probable for animals, but happens a lot in plants)
If you are asking if they 46-chromosome chimps would crossbreed with humans... well, I believe they have accumulated too much differences in their genotypes and thus would no be compatible even if they have the same chromosome number. It happens that having the same number is not the most important factor allowing or preventing species to crossbreed. There are many barriers to hybridization, e.g. the lack of biochemical recognition between egg and sperm resulting in no embryo formation... in cases that embryo is formed, it may not develop, it may develop poorly, or it may develop but the offspring comes out compromised and live shortly. Another example that chromosome number does not prevent crosbreed is the mule, which is the offspring of a female horse (64 chromosomes) with a male donkey (62 chromosomes). That's because even having different chromosome numbers, they are still quite simmilar in a genetic perspective.

All that sayd, the odds that Chimps would loose two chromosomes, stablish in the population and reproduce with humans are really really really low... I would say that's impossible. But simmilar phenomena are possible and even quite common in plants (just so you know that it exists)

If you want to learn more about chromosome number changes, I recommend this link: https://www.ncbi.nlm.nih.gov/books/NBK21229/

(Modern Genetic Analysis. Griffiths AJF, Gelbart WM, Miller JH, et al. New York: W. H. Freeman; 1999.)


Just as $k_{cat}$ represents the rate of reaction at saturating substrate concentration, $k_{cat} / K_m$ represents the rate of the reaction at negligible substrate concentration.

If we take a look at the standard one substrate/one product Michaelis–Menten kinetics rate equation:

$$v = \frac{k_{cat}[E][S]}{K_m + [S]}$$

We can imagine what happens when $[S] \to 0$, we see that when $[S] \ll K_m$, the denomiator can be reduced to $K_m$, and thus the rate equation becomes

$$v = \frac{k_{cat}}{K_m}[E][S]$$

Or in other words, $k_{cat} / K_m$ is the (pseudo-)second order rate constant between the enzyme and the substrate, when $[S] \ll K_m$.

In fact, when you get into more complex rate equations (like inhibitors, pH effects, and kinetic isotope effects) there's a decent argument (one often made by W.W. Cleland) to be made that the two key constants for enzymatic reactions are $k_{cat}$ and $k_{cat} / K_m$, and it's $K_m$ that should be thought of as the "derived" constant. (The fact that we write the rate equation in terms of $k_{cat}$ and $K_m$ is a historical accident - we could have just as easily had $ v = \frac{k_{cat}\Phi [E][S]}{K_m + \Phi [S]}$, where I've arbitrarily chosen $\Phi$ as the symbol for $k_{cat}/K_m$.)

This still leaves the issue of why $k_{cat} / K_m$ is often referred to as the "specificity constant" of the enzyme. The reason for this is that if you have a single enzyme in the presence of two different substrates, you have a competitive inhibition setup. The math is a little dense (see here or here for examples), but the end result is that the ratio of reaction rates for the two substrates is related to the ratio of their respective $k_{cat} / K_m$'s:

$$\frac{v_a}{v_b} = \frac{k_{cat,A} / K_{m,A}}{k_{cat,B} / K_{m,B}}\frac{[A]}{[B]}$$

This actually makes intuitive sense, with the right mindset - the only stage where the two substrates are competing (where you make the decision to do reaction A versus reaction B) is when they're binding to free enzyme. "The rate when you only care about free enzyme" is equivalent to the negligible substrate case. With negligible substrate, all you have is free enzyme - there isn't enough substrate to have appreciable amounts of substrate-bound form, and the rate of enzyme-substrate encounter is much lower than the rate of product formation, meaning that in the steady state you don't have appreciable amounts of product-bound form, either. Thus the $k_{cat} / K_m$ for a particular substrate is representing how good the free enzyme is at performing that reaction.


High temperatures means that lots of energy is available in the environment. This energy speeds up chemical reactions, and make possible some reactions that wouldn't happen at all at lower temperatures. In particular, proteins can adopt new shapes as temperatures get higher. It's the misshapen proteins rather than the temperature per se that kills the microorganisms.

Low temperatures mean there is relatively less energy available in the environment. This slows down or stops chemical reactions, including the ones that result in mis-shaped proteins. Extremely low temperatures may slow down a microorganism's metabolism and stop it from reproducing. That's why we keep perishable foods in refrigerators. However, if you warm the microorganisms back to a normal temperature, most of them will pick right where they left off. A few may be killed by the formation of ice crystals inside the cells that mechanically break the cell membrane.

If you walk into a microbiology lab you'll often see a wall of refrigerators, used to preserve microorganisms for later revival and use.


What is the state of automated quantitative analysis?

The word to look for is 'Image segmentation'. But also here, it very much depends on what you're looking at. Segmentation and quantification of simple fluorescence images is relatively easy and widely used. It can get very complex depending on how complex the structure is you're looking at. There are machine-learning approaches which are able to distinguish complicated structures from each other, such as different mitosis states.

Segmenting Hematoxylin-Eosin (HE) stained specimens is subject of intensive bioinformatical research. One goal is to assist pathologists in grading tissue lesions, such as in prostate cancer, but this is as far as I know not used clinically yet. Whole-slide scans of histological specimens are becoming more widely used clinically. These images are very huge (1 GB per specimen), so a research focus is also to provide a large-scale analysis of these whole-slide scans.

Also, take a look at CellProfiler (http://www.cellprofiler.org), this free open-source software saved my PhD project.

Literature I found:

Tabesh, A., M. Teverovskiy, et al. (2007). "Multifeature prostate cancer diagnosis and Gleason grading of histological images." IEEE Trans Med Imaging 26(10): 1366-1378.

Petushi, S., F. U. Garcia, et al. (2006). "Large-scale computations on histology images reveal grade-differentiating parameters for breast cancer." BMC Med Imaging 6: 14. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1634843/

I cannot provide you with a recent review, though...


How to build S16 rRNAs phylogenetic trees?

OK, first of all do not use CLustalX to align the sequences. It is a very old algorithm and is outperformed by just about any modern aligner (including its descendent, clustal omega, and t-coffee, mafft, kalign etc etc).

As for 1) that depends on what you want to do, there is no perfect solution. What question are you trying to answer? If you want a tree with species-level resolution, use all sequences. If you don't need that high a resolution, choose a representative sequence from each order or genus or whatever. In all cases, remember to use a significantly different sequence as an outlier.

As a general rule, I would use the entire sequence to build a tree, both the stems and the loops. To include structural information in your alignment you may want to check out r-coffee from the t-coffee suite.

Finally, you don't really want to use a nucleotide substitution model. Most such models assume that the sequence codes for protein and are not suitable for non coding RNAs.


Pit vs plasmodesmata

From wikipedia > pit

  Pits are thin portions of the cell wall that adjacent cells can communicate or exchange fluid through, utilizing plasmodesmata.

The definition of "pit" is therefore very related to the one of "plasmodesmata". From wikipedia > plasmodesmata

  Plasmodesmata (singular: plasmodesma) are microscopic channels which traverse the cell walls of plant cells and some algal cells, enabling transport and communication between them.

I think the following quote (from wikipedia > plasmodesmata again) will help you to distinguish pits from plasmodesma

  Primary plasmodesmata are formed when portions of the endoplasmic reticulum are trapped across the middle lamella as new cell wall is laid down between two newly divided plant cells and these eventually become the cytoplasmic connections between cells. Here the wall is not thickened further, and depressions or thin areas known as pits are formed in the walls. Pits normally pair up between adjacent cells. Plasmodesmata can also be inserted into existing cell walls between non-dividing cells (secondary plasmodesmata)

Pit field

A pit field however is just an area where there are plenty of pits! From Merria-Webster

  [A pit field is] an area in the wall of a plant cell in which one or more pits develop


These tests don't actually tell your ancestry, there is no way for a genetic test to do that because there is too much genetic variation among populations, as well as between.

Instead, the test is reporting, based on the polymorphisms observed, an estimate of their ancestry based on sharing those polymorphisms with others from a group. How do you know what polymorphisms an Asian or Native American has? Well, you do tests on a bunch of Asians and a bunch of Native Americans and use the similarities between them compared to other groups to form a 'profile' for that group. However, even an individual with a perfect geographical pedigree can share polymorphisms with other ethnic groups.

Wikipedia has a section on this:

  Many companies offer a percentage breakdown by ethnicity or region. Generally the world is specified into about 20-25 regions, and the approximate percentage of DNA inherited from each is stated. This is usually done by comparing the frequency of each Autosomal DNA marker tested to many population groups.[2] The reliability of this type of test is dependent on comparative population size, the number of markers tested, the ancestry informative value of the SNPs tested, and the degree of admixture in the person tested. Earlier ethnicity estimates were often wildly inaccurate, but their accuracies have since improved greatly. Usually the results at the continental level are accurate, but more specific assertions of the test may turn out to be incorrect. For example, Europeans often receive an exaggerated proportion of Scandinavian.[10] Testing companies will often regularly update their ethnicity estimate, changing an individual's ethnicity estimate.

In summary: ethnicity testing is at best to satisfy a curiosity. There is no way that genetic testing can identify your geneology perfectly, and in fact it is pretty meaningless to do so, because interbreeding between geographically distinct populations happens all the time.


Genes-of-interest analysis between organisms

In RNA sequencing, total RNA is extracted, then mRNAs are purified out from the sample using polyT columns (since mRNAs have a polyA tail, this will attach to a polyT DNA chunk that is attached to some solid surface). This step is necessary because ribosomal RNAs are much more abundant than mRNAs, and for sequencing you only want to use mRNAs. Then the purified mRNA is transcribed to DNA using reverse-transcriptase and finally the cDNA is sequenced.

As for microarray a set of single stranded oligonucleotids (short DNA sequences) (aka. probes) are attached to a solid (usually glass) surface as small dots. This the so called DNA/RNA-chip. Then the chip is washed with the fluorescently labelled singlestranded sample, and the complementary strands attach to each other, the rest is washed away - this is a so called hybridization technique. The signal is then detected by reading the fluorescence signals at each spot.

The microarray technique is quite old and is less sensible and the number of probes are limited / array, while with RNA sequencing you can sequence the total mRNA population of each organism and examine anything you want. Also since most sequencing techniques include a PCR step less starting material is sufficient, and has higher sensitivity and specificity.

These wiki pages on RNA-seq and microarray technique provide detailed info on both.


Abiogenesis: Beyond the research journals as a lead in to discussions on evolution

The fascinating field of abiogenesis is, as Nick Lane put it, "a wild west of ideas, theories, speculations, and even data". The stories we have involve a plethora of assumptions, there is no hypothesis where all or most of the pieces would fit together. Usually scientists agree it was RNA that played central role in the process, as the molecule could both carry the genetic code, necessary for hereditary natural selection, and catalyze basic biochemical reactions. Where the energy came from and how it was harnessed to maintain RNA (a rather unstable molecule) and perform work is still debated. A fermentation in a 'primordial soup' or a primitive form of respiration, perhaps through a thin iron-sulphur membrane, have been proposed as possibilities. The second gave a start to the iron-sulphur world hypothesis. Iron-sulphur minerals could catalyse the first organic reactions to synthetize sugars, amino-acids and nucleotides, and eventually RNA world, where natural selection could take over. Theories abound.

Usually reviews will give you a sound and approachable picture of the current thought on the matter. Take a look into Nick Lane's book and these articles, too.

Lane N., Origin of Life in: Power, Sex, Suicide: Mitochondria and the Meaning of Life. Oxford University Press, 2005. p. 94-104.
Russell, Michael (2006). First Life. American Scientist 94 (1):32.
Van Noorden R., RNA world easier to make - Ingenious chemistry shows how nucleotides may have formed in the primordial soup. Nature 2009
Check Hayden E. A never-ending dance of RNA - The recreation of life's origins comes a self-catalysing step closer. Nature 2009.
Cech TR. Exploring the New RNA World. Nobel Prize articles
Müller UF. Re-creating an RNA world. Cell Mol Life Sci. 2006 Jun;63(11):1278-93.
Lazcano A, Miller SL. The origin and early evolution of life: prebiotic chemistry, the pre-RNA world, and time. Cell. 1996 Jun 14;85(6):793-8.


This looks like a European hornet Vespa crabro to me. Wasp-like appearance, red on head and thorax and base of the abdomen. And the legs are red/dark, not yellow.

Picture from wikipedia

Hornets can be aggressive, especially if you come near the nest. Usually, European hornets are actually not really interested in people (unlike other wasps). But if there are many around your house, it is likely the nest is near, so be careful and perhaps contact the owner of the house.


Blosum matrix with probabilities instead of the positive and negative scores

Download the BLOSUM data and source-code from here. Unzip the archive which has several files.
The file called blosum'XX'.qij will have the co-occurence probabilities, and the subsitution probabilities can be calculated from them.

Also have a look at this article.


Short answer

  Do ants really find the shortest path to a food source?

No! But they can find a decent path

Longer answer

Optimization algorithms are used to search through a possibility space that is too large to explore every single possibility. Such algorithms attempt to find a good enough solution, often without necessarily knowing how 'good' the found solution is to the best possible solution. So optimization algorithms don't always find the best solution. Actually, most of the time, they do not find the best path but a good enough one in a reasonable amount of time.

Same holds true for ants. In the analogy, an ant colony is an agent based algorithm where agents leave pheromone trails. The concentration of the pheromone depends upon the length of the trail. By following the trails that smells the strongest and by regularly making small errors (so that they can keep exploring other paths), they end up with a decent solution. For more info, just google How do ants find their path?.


What is the meaning of 'state of nature' in On the Origin of species by Charles Darwin?

I would think that by "state of nature", he probably referred to any non-cultivated species. As @David suggested in the comments, the expression "in the wild" could also be a good replacement for "in a state of nature".

I think that the first paragraph you quote could be rephrased in the short sentence

  There is more phenotypic variation in cultivated species than in non-cultivated species.

My sentence is more concise but of course, is quite a bit less pleasant to read. Darwin was a very good writer after all.


While someone's ears pops with pressure, can he/she hear other sound at the same time?

Yes, of course they can. What happens when your ears feel 'full' like on an aeroplane is that the air pressure in the middle ear is different from the air pressure outside. When you 'pop' your ears, you push open the Eustachian tubes that connect the middle ear to the throat and make the pressure equal. No matter what the air pressure, the air still conducts sounds. The difference is that your ear drum moves a bit less if the middle ear pressure and outside pressure is different, thus why sound is muffled before you pop your ears.


WHO's definition about Health

  Health is a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity.

In other words, Good health means active life where you can express yourself freely, you can succeed and can make mistakes, can reach your goals, can understand your body and others, and can say no when you see your limit to yourself and others - and can set new targets to yourself, feel accepted in your society and accept yourself as you are.

Best time to Exercise for successful results in competitions - dependent on Age

Endurance atletes during ages 25-30 years in this answer about Why does max heart rate decrease with age?

Short-term and long-term effects of exercise on Vitality

There are many stages in your question in Physiology, Pathophysiology and Microbiology, for instance.
I can cover here only the surface:

very short effect of short exercise (20 min) on brain
long term effect of regular short exercise (20 min) on brain, hypothalamus and biologic clock - wakefulness (limbic system)
long-term effect of regular weekly exercise (3.5 h) on brain
long-term effect of regular weekly exercise (3.5 h) on body muscles
long-term effect of careful regular stretching and appropriate resting on congestion of body
long-term effect of regular weekly exercise (3.5 h) on metabolism
effect of regular exercise on circulation system (blood and lymph) - known to increase i.e. include temperature distribution and defence bodies distribution
short-term effect of short exercise on PTH secretion (calcium); autoregulation of renal blood flow with two major theories: myogenic mechanism and tubuloglomerular effect

where I only briefly cover one term in Pathology.
There are two unanswered questions about the renal function [Costanzo, 2013]

  (1) What component of tubular fluid is sensed at the macula densa? The
  major candidates are luminal Na+ and Cl−. (2) What vasoactive
  substance is secreted by the juxtaglomerular apparatus to act locally
  on afferent arterioles? Here, the candidates are adenosine, ATP, and
  thromboxane.

so to understand the effect of short-term morning training on PTH secretion, we should understand the two questions first.

Evidences to some things

Short-term exercise can work sometimes as prophylactics for allergic symptoms.
I think the most important thing is the irritation of your skin which is the most important endocrine organ in our body.
Skin's temperature change secretes many hormones than help us to stand irritations from the environment.

What are the effects of short-term exercise in the morning depends on the patient at hand.
I cannot say much general.
For instance, if your heart is not strained; that it has too high T peak, too heavy exercise can cause you harm.

My personal experience

Short-term exercise suited to a person with no deficits in sleeping can help to alleviate symptoms of allergies and decrease stress in a normally physiological balances without viral infections,

but the real world is not that nice.
The problem comes if the patient has any disease that uses our immune system against us such as some viral infection.
The immune response is also the source of pathogenesis for many viral diseases.
Unlike for a bacterial infection, the ultimate goal of the immune response in a viral infection is to eliminate both the virus and the host cells harbouring or replicating the virus, [Murray, Medical Microbiology, 6th ed].
Actually, some drugs are immunosuppressant like cortisone, and some procedures like radiation therapy.

However, with some medication plans, you should avoid drugs, living styles and habits that immunosuppresses your body.
For instance, HIV patients with HAART medication plan (medication combination is antiretroviral but possible immunosuppressive pathways may exist in different conditions) that involves a strategy depending on the condition, since HAART medications are life-long and cannot be stop, so other conditions etc TBC must be treated first, to avoid too much burden on the body at the same time.
In a similar way, avoiding living style or habits that puts immunosystem down can help with HIV.
Doing sport when you have slept badly many days and feel exhausted, puts your body under immunosuppression.
So the state of the disease or your physical wellbeing determines when sport is useful and when not.

Other part of your question

To hit toiled before exercise is good because then

you decrease the risk of gastrointestinal bleeding and venous congestion.
effect of exercise on constipation is one topic here; depends on you, since there are many types

The more stuff you have in your colon and gastrointestinal system, the harder it is to use fully your muscles of your body.
Try pull-ups with more empty colon vs full one.
Pull-ups require many muscles from upper trunk and lower trunk.
You cannot use all your stomach muscles if something is blocking your middle body muscles.

Good Hygiene is the easiest way to decrease the risk of any infections caused by many factors.
I estimate that 2-5 % of people visiting public toilets wash hands correctly; one video here about how one should do it.
Many people leave their hands wet.
If you have infection in your body, you should not exercise because failure to resolve the infection may lead to persistent or chronic infection or death.
It takes much energy from our body to handle with infections.
To recover from training, it requires good balance of many factors.

Summary

The best time to do sport when you are healthy

you do not have any infections (viral particularly) because a failure to resolve the infection can lead to persistent or chronic infection or death
when you have prepared early enough for the exercise with enough sleep

where pathologies and/or teratologies are not limiting your process.
You compete only against yourself and then grow from that to see you how good person you are really.

The morning exercise in a body which has rested well before the exercise and prepared accordingly to the exercise can be useful because

short-term effects on the brain (process things during exercise) (See Figure 1)
possible short-term effects during day after the exercise

and if the exercise becomes a habit in a healthy person, then

long-term effects: increased metabolism and many other positive effects described above
and many other possible reasons from social to better self-esteem

when the the person listens to his body and stops when it hurts or something goes over; can rest accordingly.
Good motivation is useful in gaining good health.
Motivation is the strength and direction of the effort.
If you are interested in morning exercise, then you can set target and make a realistic plan.
Listen your own body and be able to refit your plan accordingly.
Actually, here is an important step that the consultation of many doctors can be useful; one doctor cannot always see the main problem for instance of prolonged and deepened allergic symptoms.
Consultation and discussions of other people can also be useful - like discussing where to help for this and this; who has enough capabilities to understand it.
The person cannot always know himself what is a main disease underneath.
Anything can come that postpone some training sessions.

Sources

Infectious disease courses 2015-2016
Gleeson. The effect on immunity of long-term intensive training in elite swimmers.
Anderson. Effects of Exercise and Physical Activity on Anxiety. 2013.
Laires. Exercise, magnesium and immune function.
Gunzer. Exercise-Induced Immunodepression in Endurance Athletes and Nutritional Intervention with Carbohydrate, Protein and Fat—What Is Possible, What Is Not?
HAART and HIV in DynaMed Plus. Visited 7.8.2016.
WHO. Health Education. Visited 7.8.2016.
...


in my opinion all arthropods molt. In fact arthropods are a part of clade called ecdysozoa, the members of which undergo ecdysis (molting).

Molting is necessary because arthropods have an exoskeleton which has to be removed if the organism has to grow.


Science experiments at home with Minimal Cost

Instructions
1
Place a coffee filter in a strainer and hang the strainer over the opening of the clear bowl.

2
Slowly pour the broth into the filter, making sure that the broth doesn't overflow from the sides of the filter. If the filter becomes clogged with particles, remove the used filter, replace with a clean filter and continue pouring the broth.

3
Remove the strainer and filter from the top of the bowl and observe whether the broth appears clear (i.e., there are no suspended particles in the liquid). If particles are floating in the liquid, repeat Steps 1 and 2 using a second clear bowl and a fresh coffee filter.

4
Place the pot on the stove and pour the clear broth into the pot.

5
Add 16 ounces of distilled water to the pot containing the broth.

6
Turn on the stove and adjust the heat to medium-low. Heat the broth to a simmer (i.e., small bubbles appear near the side of the pot).

7
Add 1 teaspoon of the agar-agar powder to the simmering broth (approximately 2.5 grams) and stir the mixture until the powder is dissolved. Make sure to stir the powder to dissolve and prevent the gelatin from sinking to the bottom of the pot (where it can burn).

8
Repeat Step 7 until all agar-agar powder has been dissolved in the broth.

9
Continue stirring the broth for about 1 minute to ensure that all powder is completely dissolved.

10
Turn off the stove, place the lid on the pot and let the liquid cool for at least 15 minutes.

11
Arrange the sterile petri dishes in a row for easy assembly, but do not remove the lids.If desired, place a trivet to hold the warm pot. If you're using lidded custard cups instead of petri dishes, sterilize the custard cups by placing the cups and lids inverted (upside down) on a foil-covered cookie sheet and bake in the oven for at least one hour at 375 degrees Fahrenheit. Make sure the sterilized cups and lids are completely cooled before use.

12
Carefully touch the outside of the pot to check that it is warm to the touch and place the pot on the trivet. If the pot is too hot to touch, wait at least 10 minutes to let the pot cool.

13
Remove the lid and set aside. Place the ladle in the pot.

14
Remove the lid from one petri dish and dispense nutrient broth to fill the dish halfway. Cover the dish immediately with its cover.

15
Repeat Step 14 for each of the petri dishes.

16
Allow the nutrient broth to solidify in the petri dishes for at least 1 hour, undisturbed.

17
Gently shake the petri dishes side to side to check that the nutrient broth has completely solidified. If the broth is not completely gelled, wait another 20 minutes before checking again.

18
Cover a table or flat surface with a roll of paper towels to create a sterile work area. Tear off a sheet of paper towel and fold it four times to create a thick, rectangular wad. Set this wad on one end of the work area.

19
Transfer one petri dish to the sterile work area and remove the lid. Carefully turn the dish over and place one end on the side of the folded wad, so that it lies inverted and slightly angled (with a slight gap by the paper towel wad).

20
Turn the lid over and place it above the petri dish on the sterile work surface. If water droplets appear on the lid, gently shake this moisture off before placing on the covered surface, but do not touch the inside of the lid.

21
Repeat Steps 19 and 20 for each petri dish, positioning one side of the inverted dish on the side of the previous dish rather than the paper towel wad. The dishes will appear as a staggered set, with gaps on one side so that excess moisture can evaporate.

22
Look at the inverted petri dishes to check whether the moisture on the sides of the plates evaporated. Once all moisture has cleared, turn the plates right-side up and immediately cover with the lids for use.

23
Inoculate the nutrient agar on the plate by wiping a swab containing the desired culture on the nutrient agar surface before covering with the lid. Turn the petri dish over so that the solid is on top. Store the inoculated petri dish with the solid on top for culturing and the lid on the bottom to catch any moisture, loose particles or growth.


Is this a bed bug? I found it crawling on me in hotel bed

As already stated in the comments the animal you found is a tick (Wikipedia).

Since they are known to carry diseases you should make sure you have not been bitten or even still have one sucking your blood. So search your body. If you happen to find one still attached, do NOT squeeze it as this may stimulate fluids to flow from the tick into your body (bad). Instead get it out asap using tweezers or even better specialized tools. If you can't do it yourself ask another person preferably a doctor.

If you have been bitten watch for symtoms of an infection such as a red circle. If in doubt always see a doctor since you might require antibiotic treatment.

NOTE: usually nothing happens so don't worry too much but be alert for changes in skin around bites (if bitten that is).

EDIT: since hotel beds are not a typycal habitat of ticks you probably carried it there yourself.


That question was asked in 1953 by a classic experiment by Miller and his mentor Urey. You can find it on Wikipedia under "Miller_Urey_experiment"
Basically they zapped basic molecular building blocks to life with electricity and more complex molecules (amino acids) formed.
The experiment, with updates is nicely discussed here.
The experiment showed that the molecules required for life could be formed spontaneously on Earth from lightning. You would need amino acids, but also bipolar lipids, which can spontaneously form compartments. However, attempting to create life this way would not be worth attempting for two reasons, relating to time and scale. First (time), life has evolved only one time on Earth over 4 billion years. Second the scale of the entire Earth over billions of years is a pretty big experimental "test tube". It happened once in all this time, over all that space. A small side-issue; the fact that the codon table is optimized (and pretty universal, with only small differences), such that common amino acids have more ways to make them (more codons), and codons close to stop codons are for rare amino acids. This indicates that some early life experimented with alternative suboptimal codes that didn't make it.


How many sensory neurons are in the human body?

This is a really interesting question.  However, I'm going to try to address the context and update sections of your post rather then attempt to quantify all afferent signals in the nervous system.  This is because quantifying those signals would be an exceedingly difficult task.  It's not only logistically difficult to measure on an individual level, but to say anything definitive regarding the entire species would be superfluous.  The number of signals at any one time is constantly in flux, as not every sensory receptor generates an action potential at the same time.  Even in instances where similar or "competing" receptor types are simultaneously stimulated, those transmissions will be modulated and/or pathways suppressed.  A good example can be found in this editorial article[1] on pain, where inducing painful stimuli can alleviate an itch sensation.  I reference this to illustrate that sensory signals are not entering the brain unchecked. In the most simple of terms, they are heavily regulated.

Based on the context on your question, it seems what you really want to know is what is the maximum threshold.  In an artificial nervous system, how many signals could we pump into it before it becomes inefficient or overwhelmed?  However, what makes the nervous system unique is that it's a living system that adapts to stimuli.  When there's more signals then it can handle or process, it regulates them.  You can read more about the process and its importance in this article on sensory gating[2].  For this reason, a healthy brain that isn't being artificially stimulated shouldn't become overwhelmed.  In fact, this process makes it far more efficient then any super computer.  A fun example of this was the six chess games between Kasporov and Deep Blue in 1996.  Think of the sheer number of moves Deep Blue could calculate compared to Kasporov: hundreds of millions of moves per second.  It lost that match.  Computational capability isn't conditional on the number of inputs the system can receive, it's how that information is processed, utilized, and applied once it's in the system.

I know I didn't answer your question in regards to a hard number, but hopefully it helped give a different perspective.  Please let me know if you'd like anything further clarified.

[1]: Focus on pain.  Nature Neuroscience 17, 145 (2014). doi.org/10.1038/nn.3644

[2]: Sensory gating, inhibition control and gamma oscillations in the human somatosensory cortex.  Scientific Reports 6, Article number: 20437 (2016). doi.org/10.1038/srep20437


What does fail-safe mean in transmission at electrical synapses?

To understand what failure means in this context, we need to know a bit about how signals are communicated from one neuron to another.

Types of signals

First of all, it's important to know that synaptic signaling (communication between neurons) comes in two flavors: chemical and electrical.  The signaling is done at the interface between two neurons, known as the synapse.  There are generally dozens to hundreds of synapses between two connected neurons.  At chemical synapses, a chemical (the neurotransmitter) is released into the space between the pre-synaptic site on the axon and the post-synaptic site on the dendrite (or soma).  At electrical synapses, no chemicals are released.  Instead, porous proteins called “gap junction channels” bridge the space between the cell membranes of two neurons and create pores that allow electrical current to pass directly from one neuron to the other.

Signaling is probabilistic

Second, it's important to appreciate that neurotransmission is probabilistic, rather than deterministic.  That just means there’s a chance that signaling from an upstream neuron might fail to evoke a response in a downstream neuron.  There are several reasons why transmission is not 100% efficient, at both the pre-synaptic and post-synaptic ends.

Some of these reasons have to do with spontaneous opening and closing of channels in the membrane.  When researchers examine electrical currents flowing through single ion channel proteins they find that each channel randomly flips between open and closed states.  This is caused by molecular-scale fluctuations in the protein's shape that cause it to either block or allow the passage of electrical current (or ions).

In addition, random fluctuations in how well electrical current is able to be integrated by the downstream neuron add to the variability in signaling that makes responses probabilistic. You probably already know that "response" of a neuron refers to the firing of action potentials. And you probably also know that action potentials are generated when the membrane of a neuron becomes sufficiently depolarized - the result of a process known as synaptic integration.  A simple view of synaptic integration is the summing together of all electrical currents flowing across the membrane from different synapses in a short window of time.  If this current integrates to a total greater than some value (the firing threshold) the neuron fires, otherwise it does not.  What some may not realize, though, is that this process isn't perfect - current can leak out of the cell, other neurons can "siphon off" current, and receptor proteins in the downstream neuron can become inactive and stop contributing to the overall current flux.

All of these factors conspire together to make the signaling process probabilistic. Because there's always less than a 100% probability that signaling from an upstream neuron will sufficiently excite a downstream neuron, there will be occasions where a downstream neuron fails to fire.

So taking these things into account, we can define the following:

SUCCESS = Neuron A fires -> causes Neuron B to fire
FAILURE = Neuron A fires -> Neuron B does not fire

An example

If a synapse has 100 channels, and each channel has a 50% chance of being open at any moment, then we expect that, on average, 50 channels will be open at any given time.  If each channel can allow 1pA of current to pass through, this synapse will transmit on average 50pA of current from Neuron A to Neuron B.  Let's say 25pA is needed to bring Neuron B to threshold and cause it to fire.  Then this synapse will typically transmit more than enough current to evoke a response in Neuron B.

But here's the catch.  Because the inactivation of each channel is spontaneous, sometimes there will be more than 50 channels open, and sometimes less than 50 - just by chance.  On some rare occasions, fewer than 25 channels will be open, and if Neuron A fires at one of these crucial moments, our 100 channel synapse will transmit less than 25pA, and fail to bring Neuron B to threshold.  This is how an electrical synapse "failure" occurs. You can imagine how, evolutionarily, this might be a bad thing if that failure to fire Neuron B occurs at a crucial moment when the muscle under control of Neuron B is needed to jump out of a predator's reach.

This leads us to the question:
Given these definitions, how would we increase the chance of success, and correspondingly decrease the chance of failure?

Scaling up

Well, probability makes things a numbers game, and here's where size comes into play.  One way we could make sure that Neuron A has a really good chance of firing Neuron B is to mitigate the risk from spontaneous channel inactivation.  We could do this by simply scaling up the synapse - making it larger and adding more channels.  If we had 200 synapses, rather than 100, and they all still had a 50% chance of being closed at a given moment, then the chance becomes incredibly remote that, at a given moment, fewer than 25 channels (the number needed to fire Neuron B) are open and able to transmit signal.  This is what's meant by being made fail-safe.

It's easy to see that another means to the same end is to scale up the corresponding response in Neuron B - the EPSP - as observed at the neuromuscular junction.  By scaling up the strength of the response, it becomes less likely that random, uncontrollable influences on the cell (or muscle) would cause a failure to fire.

Hopefully, now you can see how neurons may fail to signal, and why scaling things up can, in general, make a synapse more fail-safe.


Why do earthworms have so little colour?

The reason appears to be the light cells of Hess, which are light-sensitive cells distributed over the back of earthworms, being more concentrated towards the head


Can we directly stimulate M cones in retina with current technology?

You've probably seen the news reports by now, in which researchers targeted and stimulated individual cone cells in the eyes of volunteers: "The elementary representation of spatial and color vision in the human retina" Ramkumar Sabesan, et. al. (2016). This experiment is the first time that researchers have targeted and stimulated individual cone cells. The experiments mostly involved L- and M-Cones, though the published research noted the response obtained from S-Cones, too. The researchers used 543 nm laser light (25 nm bandwidth) and an optical tracking system similar to what astronomers use to correct atmospheric distortions. So, yes, the technology exists, but it looks like it is so new in this application that no one has performed other experiments with it, yet.


Why do genitals feel frozen when freefalling?

Probably because the blood would be forced, physically, that is, by inertia to move upwards during free-fall, thus causing the genital's blood supply to become obstructed thus reducing their temperature and thus leading to the sensation of them being frozen as you described. Plus you might feel cooler all over your body due to the air flow against it and since your genitals wouldn't be as biologically favoured when your body's survival instincts for low-temperature environments kicks in you're body would probably reduce the blood flow to your genitals and other extremities favouring your vital organs such as your heart, lungs, brain, etc. with a greater blood supply to keep them warm and working.


Regulation of the replication of mtDNA at embryonic level

This is a topic which seems to be not very clear yet. References say that this is obviously dependent on the tissue and the "gene dosage" seems to play a role, and that this is probably regulated by a yet unknown factor (see "Mitochondrial DNA replication: what we know." and "Replication and transcription of mammalian mitochondrial DNA.").
Newer articles suggest that it depends also on the transcription of the mtDNA (see "The interface of transcription and DNA replication in the mitochondria." and "Mitochondrial transcription factor A regulates mitochondrial transcription initiation, DNA packaging, and genome copy number."). I will see, if there are other interesting publications, if there are problems with accessing these articles, let me know.


Why are nitrogenous bases of DNA hydrophobic if they can hydrogen bond?

These two concepts are not mutually exclusive. You have constructed a false dichotomy.  Both of these facts are true:

The electrons in the pi orbitals of the conjugated double bonds in the planar rings are hydrophobic and can "stack" on each other as shown in this drawing of a DNA helix where the bases are shown as planar rectangles:

The nitrogen and oxygen molecules (either in the rings, or as substituents on the rings) can participate in hydrogen bonds (H-bonds):

There are other examples of hydrophobicity and H-bonds co-existing.  For example on the interior of proteins.


What is the difference between "physical interaction" and "genetic interaction"?

Physical and genetic interactions are described in the help wiki, accessed via the top menu bar on the page you linked to.

Physical interactions refer to experiments where the gene product (protein) has been shown to physically interact with another protein, such as by co-immunoprecipitation, fluorescent staining, yeast two-hybrid system, etc.

Genetic interactions refer to experiments where changes in a certain gene reflect in changes to your gene of interest (or vice-versa) - dosage lethality, dosage rescue, synthetic haploinsufficiency, etc.


What are some examples of evolving networks in biology?

Others have nicely summarized to different types of biological networks and how they can evolve. I would like to make a fine distinction between evolution and dynamic adaptation and add some comments about relative evolvabilities of different biological networks.

Given an architecture, a network can respond dynamically to different inputs. The preferred paths may change and the output characteristics can vary. Example cases include the effect of environment on metabolism. Personally, I would not consider this as network evolution because the architecture remains the same. Network evolution refers to rewiring or addition of new connections.

It would be apt to classify the biological networks like this:

molecular networks

Gene regulatory networks (GRN)
Molecular (protein-protein) interaction networks (PPI)
Cell signaling networks

cellular networks

Neural networks
Biofilms (?)

organismal networks

Ecological networks (food webs etc)

There are several ways in which a network can evolve: Edge addition, edge deletion, edge modification, node addition, node deletion and node duplication.

In molecular networks edge modification happens when the chemical interaction is affected. For e.g. in a gene regulatory network a promoter-Transcription Factor (TF) interaction can change if there is a mutation in promoter sequence or in the DNA binding domain of TF. Similar situation exists in the cases of PPI and ligand-receptor interactions (Though concept of mutation doesn't apply to ligands).
Gene (node) duplications are also common mechanism of evolution of GRN. Gene deletions/inactivations also change the network and in some cases result in complex diseases. Metabolic networks evolve if an enzyme mutates and a new pathway is created.
Usually node additions rarely happen; node duplications and edge modifications are more common in molecular networks.

In neural networks the plasticity is higher than molecular networks. There is a basic architecture that is essential to support life but the connections keep changing, nonetheless, in the non-core regions. Since active neurogenesis stops after a certain point, we can assume that number of nodes remains unchanged but edge addition (new synapse), edge deletion (synaptic pruning) and edge modification (long term potentiation/depression) is quite rampant and widespread. In neurodegenerative diseases neurons die and therefore nodes are lost.

Ecological networks are affected by environment and geological barriers. So there are several subnetworks (ecosystems) that are weakly or strongly connected with each other. Introduction of foreign species (node addition) causes immediate perturbation of the local network architecture. Long term effects arise because of extinction (node deletions), speciation (node evolution leading to edge modification i.e feeding habits etc).

It is also to be noted that in all the cases the effect of a change on a network depends on which node/edge is affected; hubs are under tight scrutiny and are protected from perturbations because any dysregulation can lead to network collapse. Some networks also follow the preferential attachment behavior (which appears contradictory to hub preservation as a mechanism). I guess that molecular networks do not employ preferential attachment whereas ecological networks do.


What does it mean to use DMSO as a dissolvant in biology experiemnts?

Usually such compounds are dissolved in DMSO to make a concentrated stock solution (e.g. 1000x), which is then diluted into the culture medium. Often, the compound is soluble in water at this lower dilution, but not at the higher concentration required to make a stock. Sometimes the compound has low solubility in water and much of it precipitates. This still lets us test the effect of the fraction that remains soluble.


Blood draw from the elderly or those with tiny veins

When we need to collect blood from patients we typically draw blood from peripheral veins that are superficial. These are the veins that you can see in some individuals hands and forearms. There are superficial leg veins that are visible. Drugs like nitroglycerin or other vasodilators do not have significant effects on the superficial veins that you'd be trying to withdrawal blood from in the extremities (i.e. arms and legs).

If you wanted to really engorge someone's veins, you'd likely have to load them up with intravenous fluids. However, this would not be safe in patients needing routine blood draws; especially elderly people who might become fluid-overloaded to the point at which the develop congestive heart failure. Younger patients might temporarily have minimal increases in their circulating blood volume, but their kidneys would very quickly eliminate the excess fluid as urine.


Pianka's index of niche overlap is defined in his papers from 1973 and 1974, as:

$O_{kl}=\dfrac{\sum_i^n{p_{il} p_{ik}}}{\sqrt{\sum_i^n{p_{il}^2} \sum_i^n{p_{ik}^2}}}$

where $O_{kl}$ is the resource overlap between species $k$ and $l$, and since the index is symmetric $O_{kj} = O_{lk}$. $p_{ib}$ represents the proportion of resource $i$ that is used by species $b$. The index is a modification of one presented in MacArthur & Levins (1967).

As apparent from the formula, the only thing you need to calculate the index are estimates of resource use from the resources that both species depend on. The tricky part can be to determine how you calculate proportianal use of all resources.

I haven't used the index myself, and cannot really say anything about how common it is. I have seen references to it though. Pianka (1973) use it to study overlap between lizard species, and how the distribution of niche overlaps differ between habitat types. I haven't seen any statistical tests on it, but you should be able to use resampling or bootstrap to determine the uncertainty in the index.


From $n=2$ textbooks, the results are equivocal.

Moore et al. (2013)

There is no mention of an extensor expansion associated with the pollex.
EPL and EPB are listed as inserting on the distal and proximal phalanges, respectively.

Rohen et al. (2010) (p. 394)

"Extensor expansion of extensor of thumb" The label points to the middle of the diaphysis of the proximal phalanx. It's odd that extensor is singular here, given that there are two extensors.

However, Abdel-Hamid et al. (2013) present data from dissection of 95 limbs.

Extensor pollicis longus:

  "EPL tendon was attached to both proximal (PP) and distal (DP) phalanx through the extensor expansion in 94.7% of specimens (Figs. 1A, B; 2A). In 5.3% of upper limbs, the EPL tendon was attached to the DP through its extensor expansion (Fig. 2B; Table 2)."

Extensor pollicis brevis:

  In 55.8% of upper limbs, [EPB] was attached distally to the base of the [proximal phalanx] of the thumb (Fig. 1B). While in 41%, EPB tendon was attached to the extensor expansion of the thumb at the level of the base of [proximal phalanx] (Fig. 2A). However, in 3.2% of specimens its tendon was inserted into the extensor expansion of the thumb at the level of the base of [distal phalanx]."

And the answer appears to still be equivocal.

Abdel-Hamid GA, El-Beshbishy RA, Abdel Aal IH. 2013. Anatomical variations of the hand extensors. Folia Morphol 72:249–257.


Is it possible to insert DNA without cutting the recognition site with CRISPR/Cas9?

Look into site-specific recombination.  You can use a site-specific recombinase, specifically an integrase, that can insert a sequence of DNA at a certain attachment site.  You can add an identical attachment site into the DNA sequence to insert, allowing for the reintegration of a new attachment site.  Note however that you might get SSR onto the insertion plasmid itself, so don't do this if you need a specific amount of integration.

Look at the bottom subfigure of A for an example of integration.  Recombinases can also do other things, such as excision and inversion, based on the orientation of the attachment sites.


There are membrane proteins that act as structural components of the gap (i.e. the synapses aren't just floating there, they are anchored to each other via membrane proteins).

https://en.wikipedia.org/wiki/Neuroligin
https://en.wikipedia.org/wiki/Neurexin

The most common examples are neurexin (expressed on the pre-synaptic terminal) and neuroligin (expressed on the post-synaptic terminal). Not surprisingly, these proteins are involved in synapse formation in the developping brain, as well as the adult brain (in plastic processes where new synapses are formed). To a first approximation, as synapses are growing, their membrane proteins bind their partners and become anchored. This also leads to intracellular signalling and further maturation of the synapse. That's how synapses know where to attach.


DNA as a digital storage medium; sequences algorithmically avoided for safety reasons (or should be)?

Yes, there could be sequences that a DNA based system could not store handle/very well: repetitive DNA sequences.

Not only do such sequences make a lot of problems during the sequencing ('reading of data'), but they are also more prone to form secondary structure elements like loops, since repetitive DNA can bind to itself in various different ways. This means that similar to natural occuring repeats they are more likely to mutate during DNA amplicifation (the number of 'copies' can quite easily change), which makes the 'data' more instable.

A possible way to solve this problem would be to use specialised data formats that avoid as much Repetition of data as possible (similar to how zip or jpg files work)

Otherwise I agree with Nathan, that DNA by itself is not dangerous (since it won't do anything outside of cells, and the bacteria used in molecular biology are generally harmless unless you start eating them in large quantities or otherwise getting them in your body). The possibility that the DNA could somehow code for toxic proteins is very very low, and you could just check that the 'data' in the DNA does not form a protein by chance anyway.