Do biological phenomena follow Gaussian statistics?

kmm's answer is correct; I just want to add some of my points on what kind of data should follow Gaussian distribution.

  Unless you know from observation that a process doesn't follow a
  Gaussian distribution (e.g., Poisson, binomial, etc.), then it
  probably does at least well enough for statistical purposes.

I won't fault kmm for this statement because what they said is what happens prevalently. This is practically what all biologists do, but this is an incorrect approach.

Gaussian should not be considered a default distribution. This may lead to incorrect inferences. Usually the experimenter has an idea of what kind of data they are measuring and what distribution is the data likely to follow. If you are unsure of the underlying distribution then you should go for non-parametric statistical tests.

What kind of data follow Gaussian distribution?

According to the Central Limit Theorem, the distribution of the mean (expected value) or sum of several samples of independent and identically distributed (IID) random variables would follow Gaussian distribution. The random variable itself can follow any distribution but if you measure the mean several times using repeated experimentation, then the distribution of the mean would be Gaussian.

From the Wolfram site:

  Let $X_1,X_2,...,X_N$ be a set of N independent random variates and
  each $X_i$ have an arbitrary probability distribution $P(x_1,...,x_N)$
  with mean $\mu_i$ and a finite variance $\sigma_i^2$. Then the normal
  form variate:

  $$X_{norm}=\frac{\displaystyle\sum_{i=1}^N x_i-\sum_{i=1}^N \mu_i}{\sqrt{\displaystyle\sum_{i=1}^N \sigma_i^2}}$$

  has a limiting cumulative distribution function which approaches a
  normal distribution.

The wikipedia page on CLT is also quite good. You can have a look at it too.

Usually in biological experiments we measure some property, lets say expression of some gene. When you do several replicates, and there is no specific underlying mechanism that would generate variation (i.e. the errors are purely random), then you would get normally distributed values. Note that this applies only for the sample means. In certain cases, we assume that the variation in the value of a variable is because of some random fluctuation and therefore consider these variables to be normally distributed (not their means but the values themselves); for e.g. the weights of mice which are fed and raised equally. This is just your assumption which constitutes the null hypothesis.

Another point to note is that the variable that is expected to follow normal distribution should essentially be continuous in nature. Some discrete variables can be approximated as continuous but one should have a good reasoning of doing so. For example population sizes, though discrete, can be assumed continuous if the sizes are large.

Poisson distribution is unique and is a discrete distribution. Certain kinds of phenomena result in Poisson distributed RVs. These phenomena should basically be Poisson processes. See this post for details. Poisson distribution basically models the probability of N events in a given time interval for some given rate of events ($\lambda$). This rate is also called the intensity of the distribution.

Binomial is another unique discrete distribution. Genotypes resulting because of Mendelian segregation of genes, for example, follow this distribution. It basically models the probability of N number of events in some M trials. In binomial distribution there are only two possible outcomes. Multinomial distribution is a generalization of binomial distribution with multiple outcomes.

Since both Poisson and Binomial are discrete distributions they should not be confused with normal distribution. However, under certain conditions especially when the number of trials in Binomial distribution is high and binomial probability = 0.5 then it can be approximated as a gaussian with same value of moments. Similarly, if the intensity (rate) of Poisson distribution is high or the time interval is large, the distribution of the Poisson RV can be approximated to Gaussian (with same value of moments). In these cases, the value of the mean goes up significantly, thereby allowing a continuous approximation.

Many datasets show power-law like/skewed normal distributions and people often make the mistake of assuming them to be normal. An example (from my experience) is the expression of all the genes in a cell. Very few genes have high expression and many genes have low expression. This also applies for degree distribution of nodes in some real networks such as gene regulatory network.

In summary you should assume Gaussian distribution when:

Variable is a measurement of a value which is repeated several times from identical samples
Variability is expected to be random in the control case (in t-test, when you reject null hypothesis you are actually saying that a certain variable does not follow the normal distribution assumed under the null hypothesis)
Variable is continuous, or discrete with large sample size


Critical discussion: Gene expression and systems biology allows us to understand the control of complex traits

Turns to be too long for a comment.

If you are looking for explanation of the title/question, than it is following (roughly).

If we get information about gene expression from all different cell types, and extract also interactions between those genes (if a gets higher then b gets lower), this will allow studying multigene traits. E.g., life quality, height, mental disabilities, cardiovascular risks etc. Thing is that for most health problems that stem from single gene variation we already know named gene, or can easily find it out.

More complex issues are often hidden in statistics, links are not so clear. So, for example, autism is described by genetic variations (so far) only in less than 30% of cases or so. In other cases there is no genetic predisposition or strong evidence. Mainly that is so because many genes interact to produce final trait or illness. Looking with microscope one gene at a time will not provide information about it.

You should look into multi-gene traits, maybe pick your favourite illness (e.g. autism) and see how it is hereditary (tip: not fully). Whole-genome sequencing is important tool in tracing such issues because it gives wide overview and a lot of genetic information about patient.


Why is the floral biodiversity of grazed grassland higher than that of mown grassland?

I think you may have covered the answer in your question... but here's my take;

The 'mowing' occurs at a distinct time-point and is highly destructive and uniform, so the selection pressure is very high and only highly competitive species that are fast to grow and reproduce will be successful.

As you point out, animals will defecate and naturally fertilize the land, thus favouring growth. Other favourable factors in an agricultural environment will be that the 'mowing' will be much less uniform; the animals may favour one plant over another - so a plant that is not eaten by the animals will continue to grow and reproduce, whereas in the mowing environment this plant would not succeed; this will allow various other species to succeed where they would not in the mown environment. Also, depending how many animals are in the area the height of the grass may be higher overall, so slower-growing plants could grow enough to reproduce.


It appears to be a Noble False Widow Steatoda nobilis

From http://britishspiders.org.uk/wiki2015/index.php?title=File:Steatoda_nobilis.jpg

It apparently is thought to be introduced to the UK, and there are some reports that the bite has caused some issues for some people.

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


How much time does HIV live outside the body?

The general response to that question is not long, the HIV is a weak virus and that once exposed to air, it can survive for maybe a few minutes at best.

BUT Under specific conditions, HIV can survive for a far longer period of time, sometimes for hours or even days if the right temperatures, pH balance, light exposure, and humidity are achieved.  It is a very difficult set of conditions but is nevertheless possible.

Source : How Long Can HIV Live Outside of the Body ?

In certain conditions, the virus can survive outside the body for several weeks.
Survival depends on which body fluid it is in, volume of the body fluid, concentration of the virus within it, temperature, acidity, and exposure to sunlight and humidity.
HIV transmission has not been reported as a consequence of contact with spillages of blood, semen or other body fluids.

Source : HIV transmission & testing, Survival outside the body


About the definition of ketogenic amino acid

The fundamental 'problem' with acetyl-CoA is that it cannot be converted to glucose via the tricarboxylic acid (TCA) cycle: a two-carbon compound (acetyl-CoA) enters the TCA cycle, but two carbons are lost as CO$_2$ during each round of the cycle (in the two decarboxylation steps, ie in the reactions catalyzed by isocitrate dehydrogenase and by the alpha-ketoglutarate dehydrogenase complex).

There is no 'net gain' of carbon when acetyl-CoA is 'burned' in the TCA cycle.

This is why animals cannot convert even-number fatty acids (even-chain fatty acids) to glucose, and a basic principle of animal nutrition is that triglycerides, with the exception of the glycerol backbone, cannot be converted to glucose.

This, is seems to me, is also the key to understanding the difference between 'ketogenic' and 'glucogenic' amino acids.

Amino acids that directly give rise to acetyl-CoA (or acetoacetyl-CoA) cannot be converted to glucose but that can be converted to ketone bodies (such as D-3-hydroxybutyrate)  are referred to as ketogenic amino acids.

Pyruvate can be converted to glucose (via glucneogenesis), and amino acids that may be converted to pyruvate are considered glucogenic. A very good example is alanine which may be converted to pyruvate simply by transamination (alanine aminotransferase).

Alanine is a key protein-derived glucose precursor, especially in times of starvation (Felig, 1975). A commentary on the discovery of this key finding is given in this citation classic

In addition, amino acids that may be converted to TCA intermediates that in turn may be converted to phosphoenolpyruvate (and are thus precursors of glucose) are considered glucogenic (Lehninger, Biochemistry, 2nd Ed, 1975, p629).

We need to be aware that propionate (a three-carbon compound) is glucogenic (and this is particularly important in ruminants): it is even-chain fatty acids (and their CoA derivatives) that are non-glucogenic.

Furthermore, an amino acid may be both ketogenic and glucogenic.

Only leucine and lysine (LK) are exclusively ketogenic
Tryptophan, Isoleucine, Phenylalanine, and Tyrosine (WIFY) are both glucogenic and ketogenic
The other 14 'protein' amino acids are glucogenic

See  D'Mello (2003) for a great ref (it must be good, he's from Scotland).

The catabolism of the branched-chain amino acids (Ile, Leu, Val) provide an example of each type (Harper et al., 1984):

The catabolism of isoleucine gives rise propionyl-CoA and acetyl-CoA and is both glucogenic and ketogenic.
Leucine catabolism yields acetoacetate and acetyl-CoA (ketogenic)
Valine catabolism yields succinyl-CoA (glucogenic)

A quote from Metzler (2001) may help to clarify the origin of the terms.

  According to a long-used classification amino acids are ketogenic if (like leucine) they are converted to acetyl-CoA (or acetyl-CoA and acetoacetate).

  When fed to a starved animal, ketogenic amino acids cause an increased concentration of acetoacetate and other ketone bodies in the blood and urine.

  On the other hand, glucogenic amino acids such as valine, when fed to a starved animal, promote the synthesis of glycogen

  ... isoleucine is both ketogenic and glucogenic, a fact that was known long before the pathway of metabolism was worked out.

Thus, in feeding experiments, a glucogenic amino acid gives rise
to the synthesis of glycogen, whereas a ketogenic amino acid does not
(but does give rise to an increase in the concentration of ketone bodies)`

We may note that plants can circumvent 'the acetyl-CoA problem' as they have the enzymes of the glyoxylate cycle, where the two decarboxylation steps of the TCA cycle are 'bypassed' (the key enzymes are malate synthase and isocitrate lyase) [and plants can convert acetyl-CoA to glucose].

It is also of interest, maybe, that both arginine and taurine (not one of the 20, of course) are essential in cats (see D'Mello, 2003). Arginine is required because of an inability to synthesis ornithine and a single Arg-free meal may cause a cat to become comatose due to the build-up of NH$_3$ (see D'Mello, 2003; Bequette, 2003) , and taurine is required to prevent retinal degeneration (see D'Mello, 2003; Bequette,2003). In addition, cats need high levels of Phe/Tyr for melanin biosynthesis, otherwise hair color may change from black to red-brown (see Bequette, 2003)

Reference

Some key references given above are from the following book:

Amino Acids in Animal Nutrition (2003) Edited by J.P.F. Mello, CABI Publishing, 2nd Edition

D'Mello, J.P.F (2003) Amino Acids as Multifunctional Molecules by J.P.F. D'Mello (Chapter 1)
List Bequette, B.J. (2003) Amino Acid Metabolism in Animals:an Overview (Chapter 4)

In Addition (Taurine in Cats)

Carnivores Herbivores and Omnivores in Blondes in Venetian Paintings, the Nine-Banded Armadillo, and Other Essays in Biochemistry by Konrad Bloch


Why should we use the NA12878 dataset for benchmarking?

So to clarify for people unfamiliar with NA12878, that's the sample identification for a particular Utah woman. Her parents are NA12891 and NA12892. In human variation data-sets that's what we are given to identify individuals, an ID, sex and population. All the other data is removed to protect patient privacy. So the question is why was NA12878 (this Utah woman) chosen as the reference patient in genomic analysis...

I don't know the real practical answer but from what I gather it's inertia.

I don't have a full history for her but I do know somethings which make her genome a good choice for a benchmark. NA12878 is a fairly old to geneticists and her DNA is included in multiple legacy projects, specifically HapMap.

She has a genetic disease (CYP2D6 mutation) which is probably what initially included her and her family genetic analysis. This is a better reason to study this genome in detail instead of it simply being someone famous (i.e. Venter).

She's Utah mormon (small founder population with extensive pedigree information), has 11 children (can do recombination/inheritance analysis). What this means is that a deep understanding of her genome will have applications to this population.

Her lymphoblastoid cell line GM12878 was included as tier-1 ENCODE cell of study. This means there's terabytes of epignomic data for her as well.

When I choose to do human genome analysis, NA12878 is the obvious choice because of how much data is already available, which also means more data is going to be available. Thus I think the answer is largely inertia.

Also consider it this way, if you're trying to say your pipeline or sequencing technology is better then other ones, and everyone uses NA12878 to benchmark their technology, then it's wise to also use NA12878 so the results can be comparable.


How do trees lift water higher than 10 meters?

Disclaimer: This is not my field of research.

First, this is not a complete answer to our question. A nice explanation of the current hypothesis of water transport in trees (Dixon-Joly cohesion-tension theory, originally proposed 1894) can be found at The Amazing Physics of Water in Trees but also in Tyree (1997). The key points are that the stoma (leaf surface pores) are so small that the menisci can withstand huge water columns, that water has strong cohesive forces, and that water is transported using the negative pressure that is created by transpiration. The webpage linked above contains a beautiful visualization of how multitudes of stomata and menisci create strong negative pressures:

Second, much of the current discussion in the comments (an indication that the question might be a poor fit for Bio-SE?) revolves around the plausibility of the cohesion-tension theory, and specifically on whether water can sustain strong negative pressures. Caupin & Herbert (2006) review metastability and cavitation in water (in a physics journal), and contains experimental results on negative pressures in water. The paper references a large number of experiments under various experimental setups (I cannot fairly judge these). In their conclusion they state that:

  Among the countless cavitation experiments, only the ones with special care about water purity can reach large negative pressures; with a variety of techniques, they all obtain Pcav around −25 MPa at room temperature (see Fig. 3 (b)), which falls far away from the theoretical value (from −120 to −140 MPa). There is a notable exception: experiments with mineral inclusions achieve −140 MPa. The large gap between these data requires special attention.

So basically, the theoretical estimates lie at -130MPa and empirical results at -25MPa (-250 atmospheres), and water can clearly achieve large negative pressures. This would also mean that the current estimates are much larger than what is needed for the cohesion-tension theory to work (atmospheric pressure= 0.1MPa, negative pressure in water column at 50m ~ -0.5MPa).

They also have a section specifically discussing trees:

  7.1. Water in nature
  The law of hydrostatics teaches us that the pressure drop in a water column of 10.2 m is 0.1 MPa. This points out that negative pressures can be reached in the ascending sap of tall trees. In fact additional effects (viscous flow, drought) make the pressure in the sap negative even at smaller heights. The cohesion-tension theory, first proposed by Dixon and Jolly [56], explains that the sap column is held at the top by the meniscus in the pore of the leaves: by Laplace’s law, the meniscus curvature allows a pressure jump between the outside air pressure and the negative pressure in the sap. The trees thus contain large amounts of metastable liquids. Cavitation may sometimes occur, disrupting the liquid column and stopping the flow (xylem emboly). The complex hydraulic architecture of trees limits the damage, and strategies exist to refill the embolied xylem channels. Much work has been devoted to this topic, and is reviewed in Refs. [110,111].

There is also evidence that the risk of xylem embolism increases with tree height, and this creates a trade-off between water transport efficiency and structural adaptations to deal with embolism (Domec et al. 2008). This is for instance facilitated by the pit aperture diameter of tracheids, with apertures decreasing with height along a tree, causing increased resistance to embolism but at the same time lower water conductance. This will clearly limit the height of trees, and the paper indicates that the tallest Douglas firs are at the edge of what they can achieve.

Another recently published paper that should be relevant is 'Methods for measuring plant vulnerability to cavitation: a critical review' by Cochard et al. (2013), but I haven't had time to look closely at this. See abstract below:

  Abstract:
  Xylem cavitation resistance has profound implications for plant physiology and ecology. This process is characterized by a ‘vulnerability curve’ (VC) showing the variation of the percentage of cavitation as a function of xylem pressure potential. The shape of this VC varies from ‘sigmoidal’ to ‘exponential’. This review provides a panorama of the techniques that have been used to generate such a curve. The techniques differ by (i) the way cavitation is induced (e.g. bench dehydration, centrifugation, or air injection), and (ii) the way cavitation is measured (e.g. percentage loss of conductivity (PLC) or acoustic emission), and a nomenclature is proposed based on these two methods. A survey of the literature of more than 1200 VCs was used to draw statistics on the usage of these methods and on their reliability and validity. Four methods accounted for more than 96% of all curves produced so far: bench dehydration–PLC, centrifugation–PLC, pressure sleeve-PLC, and Cavitron. How the shape of VCs varies across techniques and species xylem anatomy was also analysed. Strikingly, it was found that the vast majority of curves obtained with the reference bench dehydration-PLC method are ‘sigmoidal’. ‘Exponential’ curves were more typical of the three other methods and were remarkably frequent for species having large xylem conduits (ring-porous), leading to a substantial overestimation of the vulnerability of cavitation for this functional group. We suspect that ‘exponential’ curves may reflect an open-vessel artefact and call for more precautions with the usage of the pressure sleeve and centrifugation techniques.


Are there any proteins assembled from non-adjacent parts of the genome?

I think that you are talking about trans-splicing. This does indeed happen. It is fairly common in protist organisms, though in humans it is quite rare. For more information about how this process works, including mechanisms in vertebrate organisms, see this paper.

Here is one model from that last paper for how it works:


What is the correct value of Neuronal Resting Potential - is it -65mV or -70mV?

Neither is incorrect. Neuronal resting potential is a function of the internal and external concentrations of ions and the conductance of the membrane to those ions via ion channels. Different neurons exhibit a range of resting potentials.

You can calculate the resting potential for a given cell using the Goldman Equation.


While the ebola virus infects a lot of human cells, immune system cells it infects are mainly monocytes and macrophages. The cells in our body mainly responsible for adaptive immunity, T cells, are at least not completely infected:

  Our data indicate that 20–30% of CD4 and CD8 T cells died during the course of infection1

That's a lot, but the ones that survive get activated and it's apparantly enough that between 80 and 10% of the infected (depending on the strain) can survive the infection. Little is known about the details of the immune reaction to ebola, but the immune system does get activated. The immune system even remains on "high alert" for quite some time after infection and recovery.

And the antibodies do stick around, at least for 10 years. Whether they confer immunity against all strains of ebola, we don't seem to know - ebola isn't very well-researched yet.


Electron Transport Chain in Mitochondria

The good ol'electron transport chain (ETC).

Before beginning let us begin by looking at the structure of a mitochondrion and the purpose of the ETC.

(source: tokresource.org)

Take of note four things:

The intermembrane space
The matrix
The electron transport chain proteins and
ATP Synthase

Now lets talk about the purpose of the ETC, essentially its job is to create a H+ (proton) gradient between the intermembrane space and the matrix it does this by taking protons from the matrix and "pumping" them out to the intermembrane space.

This creates a higher concertation in the intermembrane space and lower concertation in the matrix. This gradient will result in a process called chemiosmosis where these H+ ions (protons) will go through ATP synthase on the inner plasma membrane in order to return to the lower concentration in the matrix.

So the most important thing to note about this is that the flow of protons through the ATP Synthase is what gives it the energy necessary to create ATP.

Alright now that is out of the way lets discuss how the ETC goes about pumping these electrons out of the matrix into the intermembrane as well as how ATP Synthase works.

If you were to zoom into the area that is labeled electron transport chain proteins (that I told you to note) you would see something like this.

What we see here is that ETC is actually made up of a series of complexes (I, II, III, and IV) and a couple of "electron/reaction" carriers (ubiquinone and cyt c). These complexes and carriers are in charge of moving an electron via a series of redox reaction along resulting in the "pumping" of protons out the matrix at each complex.

*Note, understanding redox reactions help in understanding what is happening here.

The chemistry gets a little intense at this point, so I'm going to quote and link the Wikipedia article on this, which does a wondrous job explaining what occurs complex to complex.

  In Complex I, two electrons are removed from NADH [the electron carries from the previous steps] and transferred to a
  lipid-soluble carrier, ubiquinone (Q). The reduced product, ubiquinol
  (QH2), freely diffuses within the membrane, and Complex I translocates
  (pumps) four protons (H+) across the membrane, thus producing a proton
  gradient.

Note, that in Complex II no protons are pumped into the intermembrane.

  In Complex II additional electrons are delivered into the quinone pool (Q) originating from FAD [Again, electron carriers from previous steps].

Complex III receives the reduced ubiquinones from Complex I and II.

  in Complex III, two electrons are removed from QH2 at the QO site and sequentially transferred to two molecules of cytochrome c, a water-soluble electron carrier located within the intermembrane space. The two other electrons sequentially pass across the protein to the Qi site where the quinone part of ubiquinone is reduced to quinol. A proton gradient is formed by one quinol (2H+2e-) oxidations at the Qo site to form one quinol (2H+2e-) at the Qi site. (in total four protons are translocated: two protons reduce quinone to quinol and two protons are released from two ubiquinol molecules).

Finally

  In Complex IV, four electrons are removed from four molecules of cytochrome c and transferred to molecular oxygen (O2), producing two molecules of water. At the same time, eight protons are removed from the mitochondrial matrix (although only four are translocated across the membrane), contributing to the proton gradient.

NADH+H+ → Complex I → Q → Complex III → cytochrome c → Complex IV  → O2

Article here

So after all this beautiful chemistry we are left with a proton gradient. This is when ATP Synthase comes into play. Once the proton "flows" through it will bind ADP and inorganic phosphate together to form ATP.

energy + adp + pi → atp

More on how the ATP Synthase works here

This is water down in the actual chemistry portion of it but I feel like it will give you a better grasp on how it all works. If you have anyways especially regarding the series of reactions between complexes feel free to ask!


Is it theoretically possible to treat filaggrin deficiency with a dietary supplement?

I highly doubt it. Filaggrin is a human protein which is expressed in the skin and stored as profilaggrin. The profilaggrin has a molecular weight of about 350 kDa (which is rather big) and is cut into smaller units of filaggrin, which then crosslinks kreatin fibers of the epidermal keratinocytes. This enhances the durability of the skin. Mutations in the filaggrin gene have been associated with dry skin and excema. See here for more information:"Filaggrin - revisited."

To supplement the profilaggrin, you would have to bring this rather large protein into the skin. You could think about making a cream with the smaller filaggrin in it to promote crosslinking of the upper skin. The question here would be how effective such a treatment ist and how deep the crosslinking would be.


Casein proteins are soluble in milk but form insoluble curds once they reach the stomach, making it hard for digestive enzymes to break them apart. Slower digestion also is associated with delayed release of the protein's amino acids into the bloodstream.

milkgenomics.org/article/dairy-protein-digestion-life-slow-lane/

These properties of milk caseins may have evolved to benefit mammalian infants, but slowed digestion offers the benefit of increased satiety to milk drinkers of all ages. Eating foods, like milk, that take the slow lane may mean eating less food overall.

Casein proteins in milk form small spheres, called micelles, with the hydrophilic (water-loving) portions of the protein on the outside of the sphere and the hydrophobic (water-fearing) portions on the inside. With hydrophilic structures on the outside, the micelles are soluble in water (or milk, which is mostly water) [1,2].

But when the micelles reach the stomach, “one of the most ingenious events in nature takes place” [2]. The digestive enzyme chymosin snips one of the bonds on the exterior protein (known as the kappa subunit), leaving only the hydrophobic subunits inside [1]. Without their protective layer, the now insoluble proteins form a curd.

It looks like various proteolytic enzymes digest the casein 'curds' in the stomach and intestine.  "Human proteolytic enzymes were obtained in the
activated state by collecting human gastric (HGJ) and
duodenal juice (HDJ)" This is the article: In vitro digestion of bovine and caprine milk by human gastric and duodenal enzymes
Dipeptidyl Peptidase IV's  (DPP IV), a type of protease, has been shown to break down the proteins in gluten and casein. https://www.livestrong.com › Diseases and Conditions

It's in our intestine: https://www.ncbi.nlm.nih.gov/pubmed/7522442

Brush Border Enzymes & casein [that one gives me your stackexchange question!]
This article: "Effect of diet on enzymes of the brush border of the small intestine and kidney of rats" says: "Diets with low starch and high casein contents resulted in higher specific activity of leucineaminopeptidase in the small intestine than diets with high starch and low casein contents."
You can find out a bit more about that enzyme by reading the abstract of the article.
'Digestion of peptides in small intestine' in Google gives this: "The brush border of the small intestine is equipped with a family of peptidases. ... They function to further the hydrolysis of lumenal peptides, converting them to free amino acids and very small peptides. These endproducts of digestion, formed on the surface of the enterocyte, are ready for absorption."

www.vivo.colostate.edu/hbooks/pathphys/digestion/smallgut/absorb_aacids.html

[Hint - it's google searches all the way, with an occasional scholar.google search.  ... Maybe I should get back to my own work and let you all do the searches!]


This is at best anecdotal evidence. First of all, urine is, although it has been thought otherwise for decades, not sterile. The bacteria in it just don't grow under the conditions used in the lab which are used to proof bladder infections. See these two articles:

Evidence of uncultivated bacteria in the adult female bladder.
Urine is not sterile: use of enhanced urine culture techniques to
detect resident bacterial flora in the adult female bladder.

When you take into account that bacteria grow on almost all surfaces which have a connection to the outside (like mouth, stomach, gut and so on) this is not really surprising that this is true for the bladder as well.

Urine might be a relatively low risk solution of choice to rinse a wound when nothing else is available, but otherwise I wouldn't recommend it.

Then think of what urine is used for: it is the way our body excretes all the water soluble stuff it doesn't need any more. The body makes a lot of effort here to concentrate the primary urine in our kidneys to recover all the stuff which is still needed and to save water. I wouldn't drink it and make my body go through the whole process of excretion again.

About the doctors: is there any hard evidence for that or is this only an anecdote? I get highly skeptical when I hear about such stories.


Results of self-administration study about pain in honeybees?

The paper shows that honeybees prefer sucrose (sugar) solution to a sucrose+morphine (pain reducing) solution. They find that injuring the bees (i.e., potentially causing pain) does not change the relative preference for sucrose vs. sucrose+morphine, but they do eat more overall when injured.

They indirectly conclude that because the bees do not seek a pain reliever they may not feel pain of the type that, for example, mammals do. This is not the same as the ability to detect noxious stimuli (nociception), which insects definitely have, it's more about the emotional/behavioral impact. They cite some evidence that morphine could potentially have similar pain-relieving effects in insects as it does in mammals due to changes in behavior caused by morphine, but of course the interpretation of their results depend very strongly on whether this is accurate or not.

ARC is the Australian govt's funding mechanism. They don't have any commercial ties to the results of research so there is no reason to have any skepticism particular to the funding source: everything has to be funded by someone.


Are there predators evolved to eat puffer fish?

Wikipedia has some revealing information here:

  Not all puffers are necessarily poisonous; Takifugu oblongus, for example, is a fugu puffer that is not poisonous, and toxin level varies wildly even in fish that are. A puffer's neurotoxin is not necessarily as toxic to other animals as it is to humans, and puffers are eaten routinely by some species of fish, such as lizardfish and tiger sharks. Also, Japanese fish farmers have grown nonpoisonous puffers by controlling their diet.

It seems that susceptibility to tetrodotoxin varies a lot from one animal to another, and so some natural variation might allow a reasonable amount of predation to occur.  I also wonder whether the variation in the amount of toxin in the fish implies that the fish are often depleted.

There are cases of animals who have evolved a resistance to Tetrodotoxin, but for the most part its may the predators you are thinking of.  The toxin is synthesized by a symbiotic bacteria and is found not only in fugu but also blue-ringed octopus, rough-skinned newts and some sea slugs.  These animals probably all began with enough intrinsically low sensitivity to the toxin to take on the symbiont and probably evolved to be completely insensitive.  To find a predator that would have co-evolved a similar resistance you would look for a predator that particularly favors the envenomed animal.  In the case of the rough skinned newt, its suspected that the common garter snake is an example of such co-evolution. Others may be out there to discover - its probably difficult to watch marine animals to know what their typical predators are.


Is Cas9 unique in it's ability to act in response to a specific DNA sequence?

There are two classes of proteins that I can think of off the bat that are DNA sequence-specific. First are restriction enzymes, which recognize a specific (usually short) sequence of DNA and cleave it, sometimes through both strands at the same spot (blunt ends) and sometimes leaving an overhang or "sticky end".

The other class is transcription factors. Instead of altering the DNA, these proteins bind to a consensus sequence and act as a gathering point for the transcription machinery to bind and begin transcribing the following gene into RNA.

What makes the CRISPR/Cas discovery unique is that the binding sequence can essentially be an arbitrary sequence, defined by the scientist, allowing for cuts just about anywhere. Transcription factors and restriction enzymes depend on the local sequence of the DNA itself, so they only bind in certain spots.

There are other sequence-specific technologies available, such as TALEN, but they are basically a combination of a site-specific transcription factor and a fairly non-specific restriction enzyme or nuclease fragment engineered into it that cuts at a specific, user-defined site, depending on which subunits are used. CRISPR is a much more powerful (and easier to implement in vivo) technology, though, so while TALEN still has a place in the molecular biology toolbox, CRISPR is rapidly eclipsing it.


There are a variety of physiological, anatomical and behavioral adaptations that keep birds warm in winter.

For starters, birds are endothermic ("warm-blooded"), similar to mammals. You suggested that the coats humans wear are superior to feathers as insulation. Yet some of the finest coats and sleeping bags were long filled with feathers (e.g. goose down). Animals that live in cold regions tend to have smaller extremities. For example, you probably won't find many long-legged flamingos or ibises in the Arctic during the winter (though food supply is another reason they couldn't survive there).

As someone else suggested, water temperature is a relative constant, which means water (or better yet, snow) can actually insulate animals from colder temperatures.

Countercurrent heat exchange is a strategy that helps endothermic animals conserve heat. The page I linked to is part of a book titled Animal Adaptations to Cold, which includes a chapter titled "Avian [Bird] Adjustments to Cold."


Why do most plants reflect green and others other colors?

Tl;dr : Some plants reflect green while others don't simply because some plants are green while others are not.

Plants contain chlorophyll, but are not 100% made of it. Parts of the plant that contain a high amount of chlorophyll will look green, (Leaves, stem) while other parts that contain less chlorophyll and contain more of other pigments will look different. The flower looks red because it contains a lot more red pigment than any other pigments. The fruit looks yellow because it contains a lot more yellow than other pigments.
Carotene(orange) and Xanthophylls(yellow) are examples for pigments which absorb all colors except orange and yellow respectively, they reflect these colors. so it appears to be orange or yellow.

"Chlorophyll absorbs red and blue" is just another way of saying chlorophyll is green in colour.


B-form DNA is wrapped around histones in a left-handed manner resulting in a left-handed solenoidal superhelix (see that, that and this). The reason for this wrapping is that it reduces the helical tension. This post has more information about DNA helical tension. Also note that exceptions exist (i.e. right-ended direction) especially for histone at the centromere as described in this paper.

For your second question, the exact way nucleosomes are then arranged to produce the chromatin fiber is, as far as I know, still not fully understood but the most accepted model is a zigzag arrangement (Woodcock CL & Ghosh RP, 2010 and Grigoryev SA & Woodcock CL).


Do all restriction enzymes have palindromic recognition sites?

The article cited in the question goes on to discuss the different classes of restriction enzyme, for which the recognition ‘style’ differs. Not all recognize palindromic sequences.

Type II restriction enzymes

These have been divided into a number of subclasses (reviewed by Pingoud and Jeltsch). Those regarded as orthodox — which are the ones generally used in DNA cloning — appear always to require palindromic sequences in their recognition sites, although those in some other classes do not (see list here).

This statement is subject to the proviso that you regard as palindromic 5-base recognition sites, such as AlwXI, GCAGC, and others with a ‘non-conforming’ central region, such as ApaBI, GCAN5TGC. The reasons for including the latter (which provides an alternative way of defining the requirements of the recognition sequence) can be seen by examining the symmetrical manner enzymes of this class bind the site, which can tolerate a non-symmetrical central region. This is described in more detail in an answer I gave to another SE question on restriction enzymes.

Type I restriction enzymes:

  …cut at a site that differs, and is a random distance (at least 1000 bp) away, from their recognition site. Cleavage at these random sites follows a process of DNA translocation, which shows that these enzymes are also molecular motors. The recognition site is asymmetrical and is composed of two specific portions—one containing 3–4 nucleotides, and another containing 4–5 nucleotides—separated by a non-specific spacer of about 6–8 nucleotides.

Type III restriction enzymes:

  …recognize two separate non-palindromic sequences that are inversely oriented. They cut DNA about 20–30 base pairs after the recognition site.


The exact mechanism by which secretin is released is still not known.

  The mechanism by which acid brings about secretin release is not fully understood but probably involves acid sensing ion channels of the Trp family present in the brush border of S-cells.

Physiological reason for susceptibility to acid: It is because this hormone acts on pancreas and increases the secretion of bicarbonates to increase the pH. It also reduces gastric motility thereby allowing longer digestion within the stomach. So, it effectively prevents deterioration of duodenal mucosa and helps in efficient absorption of lipids by increasing ph in duodenum which is required for better action of lipases. So, its secretion is induced by increased acidity from chyme (so that it can increase pH).

Thus, we can conclude that secretin is acid sensitive.

Source: https://www.pancreapedia.org/molecules/secretin


Is the bipolar neuron of the retina considered a sensory neuron?

In short, yes. Any neuron that is involved in conveying sensory information from the periphery to the CNS is a sensory neuron. So I would consider all of those neurons in the retina sensory.

Arguably amacrine and horizontal neurons do not convey information "towards" the CNS, but they are involved in the processing of sensory information, therefore I would call them sensory. However I wouldn't split hairs about it if the consensus on amacrines/horizontals was interneurons, not sensory.

I guess the confusion is that many categories of neurons are not mutually exclusive, so neurons can be both sensory and interneuron.

Once reaching the optic lobe (I assume you mean areas in the thalamus, midbrain etc.), then the CNS neurons can loosely be classed as projecting/interneurons. Interneurons will remain within a region of the brain, often inhibiting activity in other cells within the region (or exciting). Projecting neurons will carry information to a different brain region, or back out to the periphery. These are very loose, in a nutshell classifications though.

Once you start looking at a specific region, e.g. the Lateral Geniculate Nucleus, then the neurons will be further classified, either by shape, function, neurotransmitters, inputs or outputs, or a combination of the above depending on the requirements of the system.

Edit: To elaborate, the types of neurons in the brain will usually be described in an area specific fashion, e.g. the lateral Lateral Geniculate Nucleus has 3 major classes of neurons, magnocellular, parvocellular and koniocellular, as well as some interneurons and supporting cells. Whereas about a dozen types of neurons have been described in the cochlear nuclei, including pyramidal, stellate, giant, golgi etc. But at this level, you would be looking at very specific differences that are not necessarily relevant to the pathways involved.

I would argue that interneurons are small and restricted to individual brain regions, e.g. the visual/auditory cortex, many of the neurons, e.g. pyramidal neurons in layers IV and V  are generally projecting neurons that carry information around the brain. I don't have specific numbers for percentages, but about 20% interneurons sounds reasonable to me.


Possibly, yes, but there are complications.

There are other conditions that help create the energetically-favorable conditions for bases to bind in a way to form a triplex, including acidity and presence of magnesium ions.

The region of DNA where your gene of interest lies (or its regulatory regions, depending on what you're trying to do) would need to be unpacked, as well. DNA is usually packaged into chromatin. Histone complexes, which wrap up DNA, provide some measure of protection of the major groove. To make a triplex, you'd need biochemical conditions that unwrap histones and support triplex formation, generally.

Use of RNA, specifically, could be complicated if it is or could be processed into a short- or microRNA element, which could be consumed in downregulating the population of mRNA molecules (which, in turn, ultimately regulates gene expression). It isn't helpful if it gets used up before it binds to your triplex of interest.

There is some pharmaceutical interest in TFOs (triplex-forming oligonucleotides) as a drug-delivery mechanism.

If some gene is broken and implicated in a genetic disease, say, and its DNA or nearby regulatory regions can be made accessible, perhaps a TFO can be administered that would help turn up or down the expression of that gene's protein product.

Papers on TFOs could probably point you to other engineering problems that researchers have encountered and would need to overcome in order to create an effective medicine.


Can mRNA vaccine have flaws and generate the wrong spike protein?

The mRNA won't be entirely perfect, but the imperfections will not matter.
The spike protein is big, encoded by thousands of base pairs in the virus. In the virus itself, it's not entirely homogeneous: there are always going to be small mutations that cause different variants to be produced, but nearly all of those are nearly identical.
The mRNA in a vaccine may also have some degree of copying errors introduced during amplification, which will produce some distribution of variants. Though the specifics are different, random copying errors in a synthetic process and random copying errors in natural viral replications will produce qualitatively similar types of distributions (more serious errors producing truncations and recombinations can occur in both as well, but similar arguments apply and they're even less likely to be functional).
Moreover, since only the spike protein is there, it can't actually produce a damaging infection, only teach your immune system what an infection looks like. Finally, since it's easy to validate a batch of mRNA via sequencing, ordinary quality control procedures should be fine to make sure what goes into the vial is what was planned (modulo the variances described above, when they are at a low enough frequency to fall below the threshold of discrimination).
In short: don't worry about the mRNA varying. If you're going to worry about something, worry about the virus varying enough that our nice, tightly controlled mRNA doesn't match it any more.


Are there species that occupy several roles in the food hierarchy?

Food hierarchy and food web

Ecological trophic interactions are better represented by food webs rather than simple hierarchical relationships. As a consequence, the concepts of primary/secondary/tertiary/... consumers sometimes poorly apply to reality.

Obligate and Optional

Many species are able to feed on a various source of nutrients. As a consequence, a species can be a primary consumer under one environmental condition and be a secondary consumer under another. Such species might eventually almost never be both a primary and a secondary consumer at the same time and it renders the classification of species into one or another category a little more arbitrary.

How much does one need to eat to belong to a given category?

Note also that species like the cat, for example, are generally considered as being just carnivorous while in reality they often eat a very small amount of plant material. They also indirectly consume plant materials that are present within the gut of their preys. Such cases make the categorization more arbitrary again

Examples

Primary, secondary and tertiary consumer

This one is pretty easy. Humans, pigs, bears, corvids and catfish are all examples of species that are primary, secondary and tertiary consumer all in the same time. In other words, humans are omnivorous.

I am currently preparing a stew for tonight $\ddot \smile$. There are a number of vegetables and a little bit of pork (which itself is omnivorous). Tomorrow, I'll make some salmon (which is a secondary consumer as it mainly feeds on zooplankton).

Producer and secondary consumer

Carnivorous plants are able to photosynthesize and to capture animals. Most animals they capture are often best described as a primary consumer but some carnivorous plants small fish that feed on phytoplankton or even mice and frogs according to this video.

Producer and primary consumer

Parasitic plants (such as the common holly) are able to both photosynthesize and parasitize other primary consumers (it therefore also is a primary consumer if we equate parasitism to consumerism).

The eastern emerald elysia (a sea slug) feed on algae and is able to photosynthesize (using the chloroplasts of its preys).

Producer, primary consumer and secondary consumer

I cannot think of any examples right now but I would bet that it exists (eventually in a chemoautotroph species and eventually in a species that has a various life cycle).


Why do we sweat after drinking water and running?

Exercise, such as running, increases muscle activity.  This increases the energy demand of these tissues, which increases the rate of cellular respiration.  Respiration releases heat as a by-product, therefore the body is hotter during and after exercise.

Sweating is a homoeostatic mechanism to keep core body temperature constant. It is a response to lower the body temperature. When the body becomes too hot, sweat is released onto the surface of the skin.  The water from the sweat then takes some of the excess heat energy from the body and uses it to evaporate.  Because water has a relatively large specific heat capacity a lot of heat can be carried away by this method.


A plant in my aquarium seems to be growing small plants under its leaves, what's going on?

From what I see ,it does look like some kind of Echinodorus ( Amazon sword). They do propagate by stems with new plants. They prefer to have roots in substrate.


What is the use of eye banks, if eyeball transplants do not exist at present?

You are asking two questions that you think are connected but are actually not.

  Question 1 - What is the use of eye banks?

Answer: It's to store corneas for transplant for people with cornea damage.

  Question 2 - What use is cornea transplant to a completely blind person?

Answer: It depends. If the blindness is due to clouded cornea (several diseases cause this) then replacing the cornea will reverse the blindness. If the blindness has other causes then cornea transplant is of no use to the person.


Probably don't do any experiments that involve shoving reptiles in a sack and swinging them around your head, as someone will surely call the ASPCA on you.

The type of dizziness that is associated with spinning around is called "vertigo". From wikipedia:

  Repetitive spinning, as in familiar childhood games, can induce short-lived vertigo by disrupting the inertia of the fluid in the vestibular system

So then from a physiological perspective the question is, do snakes have fluid in their ears like people do? And a quick review of snake physiology seems to suggest that they do.

Thus, I'm going to put forward the tentative hypothesis that yes, snakes can get dizzy, but it's still probably very different from you think of as dizziness.


It is not possible to do this directly. Indirectly, it is possible, this is actually done by harvesting fruits - they contain the energy of the sunlight conserved in chemical compounds like sugars or starch and their cellular structures. The basic process for this is photosynthesis.

The products from the fields are used technically to produce gas by fermentation, which then can be burned to produce electricity. Read reference 1 for more details.
What is also done is the use of sugar cane (done widely in Brazil) or corn to produce ethanol which is then used in the fuel of cars. See references 2-4.

Besides these technical processes, there is of course still the possibility to simply burn whole plants or the wood of trees, which is also the result of the fixation of sun energy.

References:

Biogas Production from Maize Grains and Maize Silage
Ethanol Production Using Corn, Switchgrass, and Wood; Biodiesel
Production Using Soybean and Sunflower
Ethanol fuel in Brazil
Corn ethanol


Seeing with one eye, why intensity doesn't get half?

Think of eyes as cameras producing an image at a given framerate. If you have 2 cameras and shut 1 of them off, that doesn't change the amount of light incoming to the other camera.

Your question is one of signal interpretation rather than receiving signals and adding them. Given that the 2 cameras have different perspectives, adding their respective pixels makes no sense. Instead, the dual images (if both cameras are on) are post-processed for spatial reference relevant to perspective.

In the case where a camera is shut off, then the spatial reference becomes a null picture and the post-processing can be skipped.

(For reference, if you took incoming data from both eyes and added them, the result would be an incoherent and largely unusable mess)


It is anthocyanins that are produced to protect the developing photosystems (chlorophylls) from being damaged by sunlight.

As you have noted, it dissipates as the photosystems become adapted to the ambient light levels. Were you able to shade your trees for several weeks, you would likely also see their leaves turn red right after you removed the shade (easily done with trees in pots). Again, it is anthocyanin positioned in the leaf in a layer above the chloroplasts, but it will not be as vibrantly red because of the green chloroplasts below.


Short Answer

Yes, autapses exist, though the role of excitatory autapses in particular is unclear.

Long Answer

A lot of your assumptions are wrong for biological neurons (I'm suspecting you have a background in artificial neural networks but that might be inaccurate). These don't directly impact your question of whether these connections exist, but I think they are important for understanding how they could function, which is just as important if not more so.

The 'refractory period' refers to a period in which a cell cannot or is less likely to fire an action potential. Cells can receive inputs freely during their refractory period.
Neurons are not single compartments. Action potentials are generated near the soma, and although they can propagate into the dendrites, synapses out on the dendrites can be fairly electrically isolated from the soma, and synaptic potentials in dendrites can take some time, easily a ms or two, to affect the soma, and they also last for several ms. They can also affect the potency of other nearby synapses.
Although axons can be cms or more in length, dendrites are rarely found and further than 1 mm from a soma in the CNS (there can be exceptions, of course; I am mostly thinking of neocortex), and most dendrites are within 100-200 um from the soma. So travel distances are much shorter than your estimate. However, synaptic transmission itself is somewhat slow, so you can add another .5 ms, and your estimate for speed is quite fast for the brain; the link you gave applies to peripheral fibers and spinal cord to brain transmission only (note they are talking about "nerves"), so your overall estimate of 1 ms from spike to autapse turns out to be reasonable, but for different reasons.
It isn't meaningful to talk about refractory periods for most synapses. Synapses can display short-term depression and/or facilitation but that isn't the same as a refractory period. Only at particular synapses containing a single release site does it make any sense to talk about refractory periods.
Cells are not activated by an individual synapse, with a few exceptions in very specialized brain areas. So just because a cell has been made to fire tells you nothing about whether a particular synapse was activated. In fact, unless that cell has fired previously very recently, you can be confident that an autapse would not have contributed to that particular firing event.

Evidence for excitatory autapses

You specifically asked about self-excitation, but it's important to know that inhibitory self-synapses also exist, and they are much more common between GABAergic inhibitory cells than between excitatory cells (Bekkers, 1998). Inhibitory autapses make a lot of functional sense because they serve as direct negative feedback.

However, excitatory autapses do exist and they may have function significance(Bekkers, 2009), rather than just being rare "accidents" that do little. In Aplysia, for example, there are autapses that cause an excitatory plateau potential during feeding behavior, maintaining activity for a long duration (Saada et al., 2009).

In mammalian neocortex, excitatory autapses have been observed but their function is unclear. Their properties can be a bit different from other synapses (Liu et al., 2013). Spike-timing dependent plasticity would suggest that autapses should shrink and go away, but they don't, which suggests they might have some functional utility, though it isn't understood yet. There are many computational attempts to find some function, which I won't list here but you can easily find by searching a reference like Google Scholar for recent articles about "autapses."

Experimentally, the role of autapses in vivo is difficult to study because there is no specific way to selectively suppress autapses outside of a computational environment, or a reduced prep where individual cells can be activated without activity in the rest of the network.

References

Bekkers, J. M. (1998). Neurophysiology: Are autapses prodigal synapses?. Current biology, 8(2), R52-R55.

Bekkers, J. M. (2009). Synaptic transmission: excitatory autapses find a function?. Current Biology, 19(7), R296-R298.

Saada, R., Miller, N., Hurwitz, I., & Susswein, A. J. (2009). Autaptic excitation elicits persistent activity and a plateau potential in a neuron of known behavioral function. Current Biology, 19(6), 479-484.

Liu, H., Chapman, E. R., & Dean, C. (2013). “Self” versus “non-self” connectivity dictates properties of synaptic transmission and plasticity. PloS one, 8(4), e62414.


Secondary signaling molecules like cAMP, Calcium, and Ras-Raf are common in many pathways and I think its a way of integrating different signals.We cannot say that at a moment only one pathway operates in a cell or a single pathway will be enough for a process to happen.I think common second messengers is a resource and time-saving method adapted by our system to coordinate different response efficiently.https://www.nature.com/scitable/topicpage/cell-signaling-14047077

Then how a cell can identify which pathway and process should go on? I think that each time this second messenger will make a small change in choosing down stream effectors.Like Calcium binds to calmodulin which in turn choose next binding partner.Maybe the number of second messengers like concentration and affinity decide which downstream effector will be appropriate for the required stimuli.You can see in this link about how different secondary messengers make different results https://www.ncbi.nlm.nih.gov/books/NBK9870/

About GPCR, more than 800 GPCR are there and you can see from this link http://jcs.biologists.org/content/116/24/4867

So, Do two hormones have the same effect on a cell if the second messenger is the same?
I think yes, see this table (https://www.ncbi.nlm.nih.gov/books/NBK21705/)

Here, from the table, you can see adrenaline and glucagon are having the same effect in the liver cell and both have cAMP as a second messenger.But in cardiac muscle and intestine, adrenaline is having a different function. So I think it depends on the cell also.


What is the name of the bug that emerging from a wood chip like cocoon?

That is a bagworm moth, in the family Psychidae. https://en.wikipedia.org/wiki/Bagworm_moth


What does “energy transfer in cells” mean?

Cells require a constant supply of energy to generate and maintain the biological order that keeps them alive. This energy is derived from the chemical bond energy in food molecules, which thereby serve as fuel for cells.

Cellular nutrients (components in foods that an organism uses to survive and grow) come in many forms, including sugars and fats, so food molecules are rich sources of energy for cells because much of the energy used to form these molecules is literally stored within the chemical bonds that hold them together.

Cells release the energy stored in their food molecules through a series of oxidation reactions. Oxidation describes a type of chemical reaction in which electrons are transferred from one molecule to another, changing the composition and energy content of both the donor and acceptor molecules. Food molecules act as electron donors. During each oxidation reaction involved in food breakdown, the product of the reaction has a lower energy content than the donor molecule that preceded it in the pathway. At the same time, electron acceptor molecules capture some of the energy lost from the food molecule during each oxidation reaction and store it for later use. Eventually, when the carbon atoms from a complex organic food molecule are fully oxidized at the end of the reaction chain, they are released as waste in the form of carbon dioxide.

They (Cells) do not use the energy from oxidation reactions as soon as it is released. Instead, they convert it into small, energy-rich molecules such as ATP and nicotinamide adenine dinucleotide (NADH), which can be used throughout the cell to power metabolism and construct new cellular components.

Sources :

How Cells Obtain Energy from Food ?
Cell Energy and Cell Functions

For more informations :

What Are Nutrients ? - Definition & Examples
Cellular energy production


What species of tree is this (found in Navarre, Spain, many tiny flowers)?

I believe you are looking at Box Elder, Acer negundo.  It's a North American species but according to Wikipedia it is naturalized in Europe.  If you search online for images, you will see the leaves and flower structures in your own pictures.  Specimens I have seen in my area (Indiana, USA) are very similar to your pictures, even identical, and the trunk is gnarly, as you observed.


Are there any sustained efforts to model existing ecosystems?

Such a model would require a fairly detailed and complete biological inventory as well as detailed knowledge of the species' interactions, and a detailed map of the physical and chemical makeup of the location or region...

I suggest reading about the The Simons Collaboration on Computational Biogeochemical Modeling of Marine Ecosystems (CBIOMES).1 This collaboration has produced ample research concerning the modeling of marine microbial communities in terms of spatial composition, metabolic interactions, nutrient flow, and seasonal variation.
Here are the research efforts highlighted on their website:

Developing New Computational Modeling Frameworks

Developing a New Trait-based Understanding of Microbial Communities Based on Metabolic and Elemental and Macromolecular Constraints (led by Zoe Finkel/Dal)
Constraint-based Modeling of Marine Microbial Community Metabolism and Physiology (led by John Casey/MIT)
Statistical Modeling of Microbial Communities: Niches, Traits, and Interactions (led by Andrew Irwin/Dal)
Thermodynamically Constrained Metabolic Networks for Ocean Modeling (led by Joe Vallino/MBL)
Models of Marine Microbial Biogeography and Biogeochemistry (led by Mick Follows and Stephanie Dutkiewicz/MIT)

Collecting and Compiling Relevant Datasets

Ocean Color and Biogeochemistry (led by Shubha Sathyendranath/PML)
Data and Tools to Define the Biogeography of Marine Microbes (led by Ginger Armbrust/UW)
Microbial Growth, Interactions and Biogeographies from ‘Omics’ Data (led by Jed Fuhrman/USC)

Bringing Together Models with Data

Advanced Statistical Analysis of Marine Microbial Systems (led by Christian Müller/Flatiron Institute)
Unifying Data and Models through Biogeography (led by Chris Follett/MIT)
Data Assimilative Modeling of Marine Ecosystems (led by Chris Edwards/UCSC)
Statistical Network Inference and Time Series Analysis (led by Jacob Bien/USC)

Concerning specific geographic sites, one of the best understood marine ecosystems is the San Pedro Channel off the coast of Los Angeles, which has been studied since 1998 as part of the SPOT project.2 Sampling efforts from this site include sensors that capture continuous in situ measurements of dissolved oxygen, fluorescence, temperature, salinity, and pressure, as well as monthly charters that collect seawater to measure nutrients (nitrate, nitrite, phosphate, silicate) and chlorophyll at 12 discrete water column depths. Peruse the publications section of the SPOT website to better understand the ecological and geochemical research that the SPOT project has enabled.
If you are further interested in the global effort to characterize and model the dynamics of marine microbial communities, I recommend a 2015 review by Fuhrman, Cram, and Needham3, which discusses methods to analyze microbial networks through space and time.

References

https://cbiomes.org/
https://dornsife.usc.edu/spot/
Fuhrman JA, Cram JA, Needham DM. Marine microbial community dynamics and their ecological interpretation. Nat Rev Microbiol. 2015 Mar;13(3):133-46.


What happens to intrinsic factor exactly at the terminal ileum, where B12 is absorbed?

After reversible attachment of intrinsic factor-cobalamin complex to its ileal surface receptor, an energy-dependent
process prevents removal of the complex from the cell surface by EDTA or acid; cobalamin dissociates
from intrinsic factor and, as suggested by previous
workers, binds to a molecule antigenically similar to
transcobalamin II; and  intrinsic factor is slowly(after some hours)degraded and forms breakdown products that are detectable in ileal extracts.

References
Textbook of Pathology Page 318

One article
Intrinsic factor mediated absorption of cobalamin

Recent articles-
Physiology of absorption of vitamin b12


Is severe but short-term pain worse than moderate but prolonged pain for the body?

The biological part of the answer to your question depends on the thing causing the pain. Burning for example, a large burn can be very life threatening biologically but small burns are not as harmful comparatively. But the psychological harm they would cause is phenomenal. This is because large burns open up the body to infections, dehydration and a lot of other harm.

Let's take stabbing as another cause of pain. One stab in a less dangerous place missing all important structures may be not that harmful but may be painful. However multiple small stabs into important structures like arteries or spinal cord could be horribly destructive.

Then let's look at headaches or nerve pain. Here it is only the pain and usually there isn't any destructive or harmful process. Most individuals would take one really, really bad headache followed by never having a headache then chronic daily "tension" headaches.
Psychologically though usually the chronic daily pain is the worst. Particularly as without adequate pain management from the start, it is less responsive to painkillers (analgesia). It frequently adds to depression if it does not cause it itself and can lead to suicide. Also painkillers themselves may cause chronic pain which does not help.

In summary, acute severe pain suggests something is seriously wrong and needs to be dealt with immediately biologically as there is likely a damaging process underlying it. However if this event is survived, it may be linked with high disability from any biological process that underpinned the pain. Chronic daily pain suggests a long continuing process. The cause of this may be life threatening, such as cancers, but is usually less dangerous at least compared to acute severe pain biologically. However the psychological aspects of this pain are seriously important as they can be particularly detrimental.


It looks very much like an immature red shouldered hawk.

  Immature Red-shouldered Hawks can be tricky to identify. Immature Red-tails show a belly band and are less heavily marked on the upper chest than young Red-shouldered Hawks.

Red shouldered hawks are smaller and like deciduous forests, like perching on wires, branches, etc. Red tailed hawks are usually birds of open spaces. They hunt from lower down than red tails, and they're often found near water (especially rivers and swamps), as they like frogs and snakes.

  Look for Red-shouldered Hawks in deciduous woodlands, often near rivers and swamps. They build stick nests in a main crotch of a large tree. During migration, Red-shouldered Hawks often move high overhead along ridges or along the coast.

Limited to a phone for a while and can't do much (I'm a dinosaur) but info and pictures here.


This is pear rust (Gymnosporangium sabinae).

It is fairly widespread in the northern hemisphere:

It is a fungal infection and affects pear trees from junipers. Pruning the affected nearby junipers can help control its spread.


How is the blood volume of a living organism measured without killing it?

Polynomial gives a good hint. By adding in a known tracer of known amount that should only circulate in the blood stream, the concentration of the tracer when completely distributed will give the volume of distribution.

If the tracer only stays in the bloodstream (and that's a fairly large IF), then the VD will be equal to the VBlood. However, as many pharmacologists know, interactions with proteins and cells can skew that number. The blood volume is also reduced by the volume of the blood cells. However, using Andrei's method of dilution, one can merely swap the cell counts with the tracer concentration.


In general

Analytic solutions only exist for special cases. Therefore a good way of approaching these problems is to first act like they don’t and be happy if you can see how to derive one. It’s also more straightforward than wild guessing.

Your problem

Notation:

$P_\text{w}$ denotes the original population and $g_\text{w}$ its growth rate.
$P_\text{m}$ denotes the mutant population and $g_\text{m}$ its growth rate.
$r$ denotes the mutation rate.

The differential equations that describe your problem are:
$$
\dot{P}_\text{w} = g_\text{w} P_\text{w} - rP_\text{w},\\
\dot{P}_\text{m} = g_\text{w} P_\text{m} + rP_\text{w}.
$$
This system of differential equations is linear as it can be written in the form $\dot{\vec{P}} = A·\vec{P}$ with $\vec{P} = (P_\text{w},P_\text{m})$ and:
$$A = \pmatrix{g_\text{w}-r & 0 \\ r & g_\text{m}}.$$
Linear systems in turn can be solved by finding the eigenvalues and eigenvectors of the matrix $A$, which are:

$\vec{v}_1 = (0,\frac{r}{g_\text{w}-g_\text{m}-r})$ for the eigenvalue $λ_1 = g_\text{m}$.
$\vec{v}_2 = \left( 1, \frac{r}{g_\text{w}-g_\text{m}-r} \right)$ for the eigenvalue $λ_2 = g_\text{w}-r$.

This means that the solution can be written as:
$$\vec{P} = c_1 e^{λ_1 t} \vec{v}_1 + c_2 e^{λ_2 t} \vec{v}_2,$$
where $c_1$ and $c_2$ are constants determined by the initial condition:
$\vec{P}(0) = c_1 \vec{v}_1 + c_2 \vec{v}_2.$
If you assume that you have no mutants at the beginning and you initial wild-type population is $1$, you have $c_1=-1$ and $c_2=1$.
With this you get:
$$
P_\text{w} = e^{ (g_\text{w}-r) t},\\
P_\text{m} = \frac{r}{g_\text{w}-g_\text{m}-r} \Big(e^{(g_\text{w}-r) t} -e^{g_\text{m} t} \Big).
$$


Well, http://meriva.org states that

Meriva® is a patented formulation of curcumin, a dietary phenolic, with soy lecithin (non-GMO)(1). The two compounds form a non-covalent adduct in a 1:2 weight ratio, and two parts of microcrystalline cellulose are then added to improve formulation, with an overall contents of curcumin of 20%

A phytosome is

[...]  a complex of a natural active ingredient and a phospholipid.
It is claimed that phytosome increases absorption of "conventional herbal extracts" or isolated active principles both topically as well as orally.
The complexation with phospholipid has been applied to many popular herbal extract or active molecules including [...] curcumin isolated from turmeric [...].

And Curcumin is

[...] is a diarylheptanoid. It is the principal curcuminoid of turmeric, which is a member of the ginger family (Zingiberaceae). Turmeric's other two curcuminoids are desmethoxycurcumin and bis-desmethoxycurcumin. The curcuminoids are natural phenols that are responsible for the yellow color of turmeric. Curcumin can exist in several tautomeric forms, including a 1,3-diketo form and two equivalent enol forms. The enol form is more energetically stable in the solid phase and in solution.

So, Meriva Phytosome Curcumin is a phytosome of curcumin developed by Meriva.


Do octopuses have better eyes than humans?

There are a couple of advantages and disadvantages of possessing the eyes of octopuses.

The first advantage of the octopus eye is that it has no blind spot. This means that octopuses can see everything that is going on in their environment, and are more aware of predators and prey than some vertebrates. Also, they have many more photoreceptors than vertebrates, at roughly 20,000-50,000/mm2 which means that their vision is much better than that of any human.
The disadvantage of the octopus eye is that it can not see in colour. The eyes possess no cones, only the invertebrate equivalent of rods. This means that  octopuses can only distinguish between light and dark.


How much of the genotype-phenotype map do we understand in HIV?

I'm sure HIV is well studied since as you know it has a small genome and is highly relevent to therapeutic research, but virus regulation can be complicated and not representative of what happens in normal cells. This is why model organisms exist. The yeast Saccharomyces cerevisiae has about 6,000 genes and researchers have systematically deleted nearly every gene and looked at what happens to the cell. This information is available on the saccharomyces genome database. For example if you search SNF1 (which has a human homolog) on SGD (https://www.yeastgenome.org/locus/S000002885). You can see the phenotypes associated with deletion, overexpression, as well as a summary of what it does and how it's regulated (with original references). I don't think it gets any better than that. A lot of what is known about genetics and molecular biology comes from studies in yeast so I think it is worthwhile learning about yeast genetics to get a better understanding of what goes on in cells.


Creation of healthy genetically modified crops

Welcome to Biology.SE.

What are GMOs?

The term 'GMO' can mean a vast array of different things and there is no objective way to distinguish what most people would call GMOs from what most peopel would not call GMOs. Humans have made 'GMO' for thousands (or even tens of thousands) of years. The detailed definition of 'GMO' will not impact the answer to the question Are GMOs safe to eat?.

Are GMOs safe to eat?

Yes, GMOs are safe to eat. There is no health risk when eating GMOs. Every scientist agree on that. Arguments saying that GMOs cause health risks have no foundation and are not based on evidence. Have a look at the Skeptics.StackExchange.com > Is Genetically Modified food safe to consume?.

Note that I am not saying that there is no discussion or debate to have around GMOs. I am only saying that these discussions have no reason to be around health risks for the consumer.

Your questions

  Could crops be made larger?

Yes. We already did that.

  Could crops become more pest-resistant?

Yes. We already did that.

  Could a 'uniform shape' be created?

I do not understand what you mean.

  Would this be done with genes from other plants? Or artificially?

The term 'artificially' has no good definition and it makes your question unclear. Most would consider pretty 'artificial' to take a gene from a species and insert it into another species (even though it occurs in nature).


Without more detail about the whole plant (including leaves), where it came from, and about whether or not it was spray-painted, watered with dyed water, etc. it would be difficult to ID.

It seems to be in the Asteraceae family, and in the pompon class, as seen in these vender's pictures. (Disclosure: I have no affiliation with the company.)

http://www.fiftyflowers.com/product/Blue-Cushion-Bulk-Flower_10.htm
http://www.fiftyflowers.com/product/Blue-Cremon-Bulk-Flowers_24307.htm
http://www.fiftyflowers.com/product/Electric-Blue-Flowers_10.htm

It is most similar to a blue chrysanthemum.

http://john-hallett.co.uk/2013/04/04/blue-crysanthemum/

Sources:

as listed above for images
http://en.wikipedia.org/wiki/Chrysanthemum (pink image)
http://www.mums.org/chrysanthemum-classes/


Why do rod cells not recover after bleaching upon exposure to bright light?

In rods, the pigment Rhodopsin can be thought of as a receptor protein with a pre-bound chemical agonist. The receptor protein is called Opsin, and the pre-bound agonist is called retinal. The absorption of light causes a change in the conformation of retinal so that it activates the opsin, causing bleaching (changing the wavelengths absorbed by rhodopsin). The bleaching of rhodopsin stimulates a G-protein called transducin in the membrane, which activates phosphodiesterase, which in turn breaks down cGMP that is normally present in the cytoplasm of the rod and is necessary for the continued operation of the sodium channel sending the neural signal.

In the dark, the channel is open and the Rods are active. In bright light, due to the amplification from cascade effects, all of the channels will be closed, stopping the Rods from sending their normal signals until cGMP levels are able to compensate.

My guess is that the bleaching ceases fairly quickly and the proteins return to their original conforms shortly, but it's the cGMP levels (remember, cGMP is destroyed, so any new cGMP replacing the old must be synthesized first) that take a long time to recover as the signal to destroy the cGMP initiates a cascade that results in strong amplifications.


Prions are fairly resistant to traditional method of sterilization.

Citing from: Guideline for Disinfection and Sterilization of Prion-Contaminated Medical Instruments

  The prions that cause CJD and other TSEs exhibit an unusual resistance to conventional chemical and physical decontamination methods. Because the CJD agent is not readily inactivated by means of conventional disinfection and sterilization procedures and because of the invariably fatal outcome of CJD, the procedures for disinfection and sterilization of the CJD prion have been both cautious and controversial for many years.

The same paper also lists several effective and ineffective methods for sterilization (efficient method have > 3log10 reduction in prion content within 1 hour)
I am not going to list them all here but you can see Table 2 in the paper.

Just to answer your specific question about oxydation, certain oxydising agents are effective, others are not. Similarly certain autoclaving (=sterilising with heat) procedures are fine and others are not.

Another interesting paper Methods to Minimize the Risks of Creutzfeldt-Jakob Disease Transmission by Surgical Procedures: Where to Set the Standard?


How often does bacterial transformation happen?

Transformation underpins a lot of lab modern projects.

This will be a very unsatisfying answer, and this wikipedia entry explains why. The time, and success, of bacterial transformation of competent cells varies greatly depending on a few things mainly:

the length of nucleic acid sequence for insertion (or more accurately, the plasmid)
the species of target organism (or more accurately, the genotype of the target organism)
a host of other things

With a specific plasmid and organism you would be able to get a more satisfying answer, but I imagine the answer would even differ from lab to lab.

I worked with a microbiologist that provided me with a protein as a part of my honours project, and I can give you a broad impression I got from them: it does not happen often. Sometimes none of the cultures you are trying to transform will incorporate the new sequence into their genome, other times the cloning process goes very well and all your cultures will be transformed successfully. For our project, valid colonies only presented after a week with reasonable success (more than half the attempts were successful). But you don't know if the transformation worked until way after the first transformation happened.

The mechanisms behind this are grossly understudied. If we take some thing B. subtilis, arguably the most academically studied organism in the field of transformation, it can take up the DNA as food or incorporate it into its genome but nobody knows exactly how this happens at a molecular level (Chen & Dubnau, 2004)

Chen, I., & Dubnau, D. (2004). DNA uptake during bacterial transformation. Nature Reviews. Microbiology, 2(3), 241–9


What is the simplest way to demonstrate the germicidal property of UV light?

You can make homemade bacterial growth medium.

https://www.madaboutscience.com.au/shop/science-extra/post/grow-bacteria-on-homemade-agar-plates/

Basically it is just nutrient jello: beef stock, sugar, gelatin to make a firm surface.  It would be nice to have all your cultures in uniform plates or cups.  You could order petri dishes or use what you have available.  I would consider an ice cube tray or you could cut off disposable Red Solo cups to make dishes.

Then forget e.coli.  Inoculate the dishes with random things in the environment.  Everything has microbial life.   Fingerprints from various people are fine. Tongueprints would be a good variation - the jello is not poisonous.   A paw print from an animal would be fun.  A stick from the yard.  A snail.  Label each one with a label you can see from above - maybe a piece of paper on the table next to it.

Each of these prints will grow a mixed bunch of germs and fungi.  You might want to keep them cool because they will grow fast.  Take pictures periodically over time.  Keep them covered so they don't dry out.

Each type of dish (for example, Ted's tongue print) will have one dish in the dark (under foil) one in the light and one under UV light.  If you make big dishes you could have a half and half: light side and dark side.

Count colonies that can be seen at each time period.  That is your hard number and you can graph it over time.  The lines will diverge which will be a great visual.

In addition to the inhibitory effect of UV you can discuss how it differs.  Suppose there are orange colonies which do not seem to be inhibited by UV in the same way as everything else.  You could smear some of the orange on a microscope and look it is.  Is it some resistant organism?  You could discuss the variety of colonies that appear depending on the inoculum.


What are these two nerves running parallel to the spine called?

From this closeup image, you can see there is more than one nerve on each side that is parallel to the spine.

Source: imgur.com

First, they are the right and left sympathetic trunk that run from the base of the skull to the coccyx.

Image source: Earthslab.com

Additionally, they could be the right and left long thoracic nerve, which innervate the serratus anterior muscles in the chest wall. In your image they appear like running along the spine, but in reality they run vertically and laterally in the chest wall.

Source: Semantic Scholar


What causes plants in the prunus genus to reach anthesis?

Here’s how it works. Every morning when the sun breaks over the horizon — no matter what time of year it is — a clock starts ticking inside the trees. After a specific number of hours, the plants’ cells start producing high levels of a molecule known as the FT protein. This protein is responsible for initiating processes that help the plant grow.

But the FT protein has a curious property: In the absence of sunlight, it curls up and dies. So when the sun sets, it degrades rather quickly and becomes useless to the plant.

Nilsson thinks this peculiarity is the key to the seasonality of certain flowering plants, including most trees that blossom in the spring.

If a plant is genetically programmed to produce lots of FT protein starting, say, 13 hours after dawn, the molecule will be abundant during the last few hours of daylight in the longer days of summer. And those few hours are enough to kick-start crucial growth processes. So the cherry trees do most of the heavy lifting for the spring festival — bud and flower formation — way back in the summer and early fall.

As autumn progresses and the days shorten, that same 13-hour clock — the number of hours will vary by species and even by individual plant — means that the FT protein will be produced in darkness, and it will degrade before it can work its magic. The trees take this as a signal to drop their leaves and stop generating new buds.

When winter arrives, day length and temperatures both reach their annual nadir. At this point, the plant goes through vernalization, a dormancy period that has enormous importance in protecting the trees, for reasons explained below.

In springtime, one might imagine that the FT protein process would reverse: The days get longer, the FT protein is produced during daylight hours, and the plant kicks off its growth process. Surprisingly, that’s not what happens.

While the cherry trees recognize the arrival of winter by sensing a decline in daylight, they detect the arrival of spring based on temperature. They wait for what’s called a “temperature sum”— basically a bunch of warm days in a row. (The precise temperatures and durations required vary by plant.) When the temperature sum is reached, the blossoms open. Of course, since the National Park Service can’t control the weather, peak blossoming doesn’t always coincide with the Cherry Blossom Festival’s lighting of the stone lantern and the Japanese taiko drummers.

The cherry trees’ habit of marking the start of winter by daylight and the end of winter by temperature is reversed in some other plants. Plant biologists, for example, base much of their genetic research on Arabidopsis thaliana, or mouse-ear cress, a small plant that belongs to the same family as cabbage. (“It’s the laboratory rat of the plant world,” says Nilsson, because its small genome enables researchers to closely observe its genetically based behaviors. ) The plant measures the arrival of winter by a drop in temperatures and decides when to flower in spring by day length.

Click here for the source of this information, hope this helps :)

-Sartoaster


What is a substance that is safe to eat, not absorbed and not metabolized?

Simethicone is one example. It is a mixture of silica gel and dimethicone (polydimethyl siloxane); they are individually inert too.

Simethicone/dimethicone is used as antigas (they help the gas bubbles coalesce). It does have a laxative effect, though.


Why are people unable to develop lasting immunity against Norovirus?

So the direct mechanisms of norovirus immunity aren't well understood - the shortage of straightforward animal models, and the extreme difficulty in culturing the virus make mechanistic studies really rather hard.

A modeling study pegged the duration of immunity at 4.1 to 8.7 years when talking about symptomatic disease, which is much higher than many of the estimate's you've encountered, and isn't actually all that fast. The older estimates were built off human challenge studies, which involved massive doses of norovirus, rather than the normal exposure you'd have. Now that is for a single strain, but immune cross-reactivity for strains isn't well understood. There's also several efforts to develop norovirus vaccines, which suggests some duration of immunity is at least possible. It's also possible that a proportion of the population (~20%) is simply immune due to the absence of the FUT2 gene, which acts as a receptor for the virus in the intestines.

In addition, there's definitely some antigenic drift, where mutations in the primary antigens negate previous immunity to the disease (the same mechanism that causes you to eventually lose immunity to a particular strain of influenza).

This paper is a pretty brief review of all these factors, written by some norovirus experts.


Yes plants can absorb organic compounds..For example plants can absorb citric acid

Due to citric acid’s ability to chelate metals and be absorbed by plants, it is hypothe-sized that exposure to it will increase the ability of wheat-grass  to  absorb  macro-  and  micro-nutrients,  as  well  as  heavy metals, from soil.

Citric acid chelates absorption
Also plants have the ability to absorb and release sugars.

Plant roots are able to absorb sugars from the rhizosphere but also release sugars and other metabolites that are critical for growth and environmental signaling. Reabsorption of released sugar molecules could help reduce the loss of photosynthetically fixed carbon through the roots

Monosacharid absorption activity
I'm sure there are other examples, feel free to edit the answer.


What is the instructional language of DNA?

This language is called the genetic code. But before talking about this specific code, it is important to talk about how the code is read. Please note that the below answer is a simplification of the reality.

Mechanism by which the code is read

To make things easier (reality is a little more complicated), DNA is "formatted" into RNA which is then "formatted" into proteins. When "formatting" occurs, we do not lose the previous format but we only copied the information into a new format. The formatting from DNA to RNA is called transcription and the formatting from RNA to proteins is called translation.

Proteins are the active units that affect cell activities. The activity of the proteins is a function of their sequence. As a consequence the language/code we must understand is the relationship between DNA and proteins.

Numeral systems of DNA

DNA, as you said, is written in quaternary (=numeric system at base 4). The four letters are called A, T, C and G which stands for Adenine, Thymine, Cytosine and Guanine (4 nucleotides).

Numeral systems of proteins

Proteins, on the other hand, are coded in a system at base 21 (21 amino acids).

Redundancy

Because $4^2=16<21$, we need to use (at least) 3 letters in DNA to code for 1 amino acid. Because $4^3=64>21$, we necessarily have several codes of 3 nucleotides that match to the same amino acid. We talk about redundancy. In computer science, a byte is a series of 8 bits. In biology, a codon is a series of 3 nucleotides.

Code

Below is the code:

, where Phe, Leu, Ser, etc... are an abbreviation for specific amino acids. Phe for example is the phenylallanine.

As you can see in the above table, most of the redundancy is caused by changes in the third letter of the codon. More information on why it is the case on this post.

There are 4 special codons.

AUG: Is the start codon. It is an indication of where translation should start.
UAG, UAA and UGA are stop codons. They are an indication of where translation should stop.

Possible confusions

Central Dogma of Molecular Biology

The unidirectional relationship between DNA, RNA and proteins has been called Central Dogma of Molecular Biology. Of course, there is no place for dogma in science and the term is very improperly used. Interestingly enough, the Central Dogma of Molecular Biology is partially wrong because this relationship between DNA, RNA and proteins is not necessarily unidirectional. The reverse transcriptase is an enzyme that reformats DNA from RNA.

Genetic code

If you google "genetic code", most hits will display the letter U instead of the letter T. The reason is that the code is often presented for the relationship between RNA and DNA and the only difference in the code between RNA and DNA is that T (Thymine) is replaced by U (Uracile).

mRNA vs RNA

Not all RNA are meant to be translated into proteins. Only mRNA (m stands for "messenger") are. For example, the process of translation is itself catalyzed by RNA (called rRNA, where "r" stands for "ribosomial")

Note also that DNA is first transcribed into pre-mRNA which is then modified into mRNA before being translated.

Is all of DNA transcribed?

No. In eukaryotes (which include pretty much all the living things you may think of to the exception of bacteria and viruses), most of the DNA is not transcribed. The rest is used for regulatory purposes or might not be used at all. The regions (called locus/loci) of the DNA that is being transcribed are called genes


What is this red mushroom with the "inverted" cap?

Looks like Sarcoscypha Austriaca (scarlet elfcup). It's actually used in many textbooks as a representative species for the Ascomycetes.

Details from Wikipedia and Messiah.edu both confirm that this species is found in Europe and that it is typically found either as solitary or clustered fruiting bodies (2-5 cm wide) growing among rotting wood matter in damp wooded floors in the spring.

Photos below:

 Source: Wikimedia

 Credit: William Roody; Source: Messiah.edu

Read more at MushroomExpert.com.


Nice find! That most definitely is a Poekilocerus pictus, also known as a "Painted Grasshopper".


Approximately how thick is a single strand of cat (domestic housecat) hair?

There are a few different types of hair on a cat.  But I think you are referring to the down hair on the cat.  It will also vary on the breed of domestic cat.  As a general statement, you can find a lot of quirky characteristics of mammals by looking at early genetics papers where people where trying to find genetic elements to obvious phenotypes.

For the down hairs, you can see "The ‘rex’ type of coat in the domestic cat."
Journal of Genetics [0022-1333] Searle, A G and Jude, A C yr:1956 vol:54 iss:3 pg:506

Table 3. Thickness in µ of normal and rex down-hairs

[Type of Cat][Diameter in um][SE of Mean]

Normal          25.8;   1·32;

English rex     16·2;   0·54;

German rex      17·0;   0·50;


Very high 260/230 absorbance ratio of an RNA sample

Gergana is right about the effects of the Guanidine isothiocyanate, but not the details there of.  Guanidine isothiocyanate absorbs strongly at 260 and NOT 230 (guanidine hcl is the one that absorbs strongly at 230).  As such if your RNA is highly contaminated with guanidine isothiocyanate, which is used in at least one buffer in just about every RNA prep kit, your 260/230 is going to be much larger then 2 (also the "concentration" will be artificially high.  So if you are getting a 260/230 of 25 and have a "concentration" of "1000 ng/µL" you may actually have less then 200 ng/µL of RNA and a ton of Guanidine isothiocyanate throwing everything off.)


Do homing pigeons fly straight home or follow certain "highways"?

They have mental maps of landmarks, which they use as well as "compass" cues:

  ... experienced birds can accurately complete their memorized routes by using landmarks alone. Nevertheless, we also find that route following is often consistently offset in the expected compass direction, faithfully reproducing the shape of the track, but in parallel.

--Pigeons combine compass and landmark guidance in familiar route navigation

Landmarks are more important than compass cues in general, and pigeons develop their own landmark maps:

  we show that homing pigeons (Columba livia) not only come to rely on highly stereotyped yet surprisingly inefficient routes within the local area but are attracted directly back to their individually preferred routes even when released from novel sites off-route. This precise route loyalty demonstrates a reliance on familiar landmarks throughout the flight, which was unexpected under current models of avian navigation.

--Familiar route loyalty implies visual pilotage in the homing pigeon

That means that different birds do use different routes:

  Here, we demonstrate that birds develop highly stereotyped yet individually distinctive routes over the landscape, which remain substantially inefficient.

--Homing pigeons develop local route stereotypy

In fact the same bird might use different routes over time as it learns new landmarks:

  a wide intraindividual variability was observed in repeated tosses at the same site; some pigeons remained faithful to the first route, whereas other birds tried successive new routes which, in most cases, were significantly shorter than previous ones. This result indicates that pigeons try, and are actually able, to improve their performance in subsequent releases from the same site.

--Pigeon homing: The influence of topographical features in successive releases at the same site


Which information can be extracted from time course RNA-Seq Data?

It can be complicated because RNA-seq data is looking at gene expression, in the form of mRNA. But there are thousands of housekeeping genes that are expressed constantly, as long as an organism is alive. So the real interesting genes in a time course are those that are differentially expressed. So gene 1, in your example is not that interesting. Gene 2 however shoes a 4-fold increase between day 50 and day 100. Still, that is not that huge. You need computer programs to sort all this out. But what you want is to be able to associate a huge change in mRNA (gene expression) that can be distinguished from background.


Why is the vermis of the cerebellum associated with speech?

Although speech production is in generally executed in the cerebral domain, the dysarthria resulting from damage of the vermous is a symptom of the resulting general muscle weakness. So yes, you get slurred speech because your muscles are weak, but the weak muscles certainly aren't ever isolated to speech production.


At least some plants have cellulases which can be used to cleave primers from mature cellulose chains.
Cellulose synthesis requires chain initiation and elongation (the two processes are separate). CesA glucosyltransferase initiates cellulose polymerization using a steroid primer and UDP-glucose. Cellulose synthase utilizes UDP-D-glucose precursors to elongate the growing cellulose chain. In some plants cellulase is then used to cleave the primer from the mature chain.
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4119035/