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qPCR: Accounting for different sample mass when interpreting and comparing Ct
I'm trying to use qPCR to quantify the amount of a specific bacteria species in patient sputum, but I don't really have the option to use consistent quantities of sputum to elute DNA from. The qPCR works fine, but once I have the Ct results, what is the best way to account for the fact that I'm using different masses of sputum?

Are you always using a specific amount of DNA from your samples (i.e. 10 ng) or a relative amount (i.e. 10% of yield from one sample)? This make an important difference in how you can/have to normalise your results.

Relative amount, like 10% of the yield from a sample. We expect human DNA and DNA from other bacteria to be in the sample, so diluting all samples to the same quantity of DNA may not be useful to us.

If you are always using a relativ amount of your input yield for each sample, then you'll need to correct your Ct values for the absolute DNA yield of each sample. If you can't measure the DNA yield of each sample, then you'll just have to assume it is directly dependent on the sputum input mass. This assumption is pretty faulty though, since direct DNA measurements are much more exact and are not affected by biases from DNA extraction efficiency differences or batch effects.
Since Ct values represent a single qPCR cycle in the linear phase in which the target DNA is doubled, you need to adjust the CT values by +1 for samples with half DNA input and by -1 for samples with double input (or generally $Ct_{adjusted} = Ct - log_2(inputfactor)$ ). Of course this method of normalising assumes that the relative content of your target DNA in the sample is independent of the total sample yield (which may or may not be true; if your specific bacteria species is proliferating a lot more in one patient compared to the other this might affect both relative and absolute DNA amounts).


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Why the position of facial organs is the same for almost all animals on Earth?
I was questioning myself on why the position of facial organs (eyes, nose, mouth) is the same for almost all animals on Earth ? Is it because of a common ancestor in evolutionary history ? We don't see animals with a mouth on the forehead and eyes on the chin. This face pattern looks universal, is there some biological cause behind, natural selection?

There is more diversity than you seem to acknowledge. Consider octopuses, spiders, sea stars, slug, etc... Also, how you define these organs is up to subjectivity. For example, insects have amazing chemical sensory organs on the legs but you probably will not want to call these organs noses, just because it is not in the middle of the face.

That being said, the question of how much of it is due to common ancestry and how much of it is due to some selective pressures is still of interest. It appears for example that a head like structure appeared several times in independent lineages if I am not mistaken.

If those organs were elsewhere, wouldn't you just call that area the "face"?

Maybe I misused some of my words and I know my statement don't apply to all animals, but for example if you take a human, a bear, a squirrel, a tiger, a goat, etc.. the head structure looks similar (eyes on top, nose below and then the mouth). I know that I simplify a lot but it's to be able to easily explain my question.

@Jagoe Thank you for your answer, actually cetaceans seems to be a very good example.
And so, is there a constraint reason that could explain why mammals usually have eyes above the mouth ?

Most mammals live on land where obstacles to vision come from below (eyes up top see over barriers) and food tends to be low rather than high. Selection pressure would have to outweigh those simple facts.   Mammal eyes are in very different spots though. For a cat or human the eyes are in the front to assist depth perception. For a cow they are on the sides so they can see predators from any direction.

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Expected reproduction rate of a dandelion and/or fern
I am working a basic mathematical/computer simulation of an ecosystem, and I need to know the birth rate of each organism in my simulation. However, I could not find any data for how often a small, asexually-reproducing plant, like a fern or dandelion, reproduces. Does anybody know either a) the time to reach sexual maturity and the expected offspring of one dandelion or fern OR b) when starting with one plant, the expected living dandelion or fern plants after a year?
In other words, if I plant one dandelion or fern in a closed system (providing it with requisite water, food, sunlight, etc), how many can I expect to find at the end of the year?
These values don't have to be exact, I can adjust them later, but I need something to use as a baseline.

Dandelions may have "from 54 to 172 seeds per head and a single plant can produce more than 2000 seeds" (https://fyi.uwex.edu/weedsci/2002/11/12/dandelion/), but the number of inflorescences depends, for example, on the age of the plant. It should also be remembered that some individuals repeat the blooming in autumn, although it is not so abundant (usually only one inflorescence). That, what is called a dandelion (Taraxacum officinale) is a collective species, which actually consists of several hundred microspecies, which may differ in the amount of seeds produced. Thus, the given data is only quoted.

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Why would it be beneficial for cortisol and corticosterone to exhibit pronounced anti-inflammatory activity?
These questions are always a little silly (as we will never truly know), but it always struck me as odd that corticosterone and cortisol exhibit pronounced anti-inflammatory activity.
Because these compounds are released during fight-or-flight episodes, it seems almost counter-intuitive for an organism to promote "anti-inflammatory activity" during an event that is most likely coincident with injury (i.e. wounds from fighting / escaping).
Anti-inflammatory activity, I believe, is fairly synonymous with anti-coagulation activity. If wounds are most likely to occur during periods of fight-or-flight (which is a reasonable intuition), why would organisms select for a glucocorticoid that has additional effects such as reducing acute clotting capacity?
The only thing that I can think of is there is an energetic cost to initiating the coagulation cascade, which would siphon energy away from skeletal muscle. Any thoughts / hypotheses?
Cheers~

Interesting question. It's easy to imagine why you would want to suppress inflammation in a fight-or-flight situation. Inflammation can cause painful swelling, fever, and it can dull mental acuity, all of which might hurt your chances of a win or escape.
After a little PubMed search, it looks like sympathetic adrenal responses (like cortisol) can actually induce a net hypercoagulability of the blood (1). So, even though inflammation does induce coagulation, it looks like the sympathetic anti-inflammatory response is not necessarily synonymous with anti-coagulation. This also makes sense in the context of Cushing's Syndrome, where hypercoagulation is associate with elevate cortisol levels, among other factors (2).


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What is the historical justification for the 'per 100 gram of tissue' term in the units of cerebral blood volume?
The title of this post pretty much says it all. I've looked around quite a bit for the original paper that invoked the decision to normalize a fluid volume to $\frac{1}{100 \text{ gram}}$. I thought that some early infrared spectrophotometry studies (which I believe are the first quantifications of CBV) would explain this...but they do not. Perhaps this is related to a more general (and older) approach to perfusion quantification methods, but I really do not know.

I’m voting to close this question because it is a question about the history of science, and should be translated to the eponymous SE site.

The below is speculative, but I believe it to be approximately, if not entirely, correct.
The origin of this 'unit of reporting' appears to stem from the original attempts of Kety & Schmidt to provide the first quantitative measurement of cerebral blood flow (CBF). There are a few papers spanning several years...with the first one coming out in 1945...but the most relevant one that provides some insight is here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC439518/.
They provide a logical derivation that uses some basic calculus and laws of incompressible fluid flow to produce the following equation:
$$\text{CBF}(\tau)=\frac{\frac{Q_B(\tau)}{W}}{\int_0^{\tau}\left[A(t)-V(t)\right]dt}$$
, where $Q_B(\tau)$ denotes the number of N2O atoms in the brain (we will use the SI unit $\text{mol}$ to report this value), $W$ denotes the whole weight of the brain, and $A$ and $V$ represent the arterial and venous concentrations of N2O, respectively. The authors' derivation to this point in the paper is well explained, and the corresponding physical dimensions of CBF are easily tracked as being: $\displaystyle \frac{\text{volume}}{\text{time}\cdot\text{mass}}$.  If we choose centimeters cubed ($\text{cc}$) as our unit of volume, minutes ($\text{min}$) as our unit of time, and grams ($\text{g}$) as our unit of mass, then the dimension are more specifically written as: $\displaystyle \frac{\text{cc}}{\text{min}\cdot\text{g}}$. So far, so good...but where does the $\frac{1}{\text{100 g}}$ come from?
Their derivation continues with the following claim:

For long enough $\tau^*$, $\frac{Q_B(\tau^*)}{W}=V_{\tau^*}S$, where $S$ is the partitioning coefficient of N2O between the brain tissue and brain vasculature.

With no additional explanation, they then write:

By substituting appropriately and multiplying through by 100, one obtains a value for cerebral blood flow in convenient units: \begin{align} \text{CBF}(\tau^*)=\frac{100 V_{\tau^*}S}{\int_0^{\tau^*}[A(t)-V(t)]dt}\end{align} where CBF is expressed as cc. of blood flow per $100$ g. of brain per minute

These final steps are missing quite a bit of explanation...so here is my attempt at justifying the steps. Firstly, returning to the claim that:
$$\frac{Q_B(\tau^*)}{W}=V_{\tau^*}S \quad (\dagger_1)$$, you should immediately see that the physical dimensions do not match up (and therefore, the equality is invalid). On the left side we have $\displaystyle\frac{\text{mol}}{\text{g}}$, and on the right side, we have $\displaystyle\frac{\text{mol}}{\text{cc}}$. Importantly, though, we can write out these units a tad more informatively:

$\displaystyle\frac{\text{mol of N2O in brain tissue}}{\text{g of brain tissue}}$

$\displaystyle\frac{\text{mol of N2O in brain vasculature}}{\text{cc of brain vasculature}}$

Next, note that $S$, by definition, has units that can be represented as:
$$\frac{\frac{ \text{mol of N2O in brain tissue}}{ \text{cc brain tissue}}}{\frac{ \text{mol of N2O in brain vasculature}}{ \text{cc of brain vasculature}}}$$
Now, returning to $(\dagger_1)$, if we write out our more descriptive units we have:
\begin{align}\frac{Q_B(\tau^*)}{W}\frac{ \text{mol of N2O in brain tissue}}{ \text{g brain tissue}}&=V_{\tau^*}S \frac{\text{mol of N2O in brain vasculature}}{\text{cc of brain vasculature}} \cdot \frac{\frac{ \text{mol of N2O in brain tissue}}{ \text{cc brain tissue}}}{\frac{ \text{mol of N2O in brain vasculature}}{ \text{cc of brain vasculature}}}\\&=V_{\tau^*}S\frac{ \text{mol of N2O in brain tissue}}{ \text{cc brain tissue}}\end{align}
Notice that we still have this issue of physical dimension mismatch...however, if we approximate the density of the brain tissue as being largely similarly to water, then we know that water has the density of $~1.0 \frac{\text{g}}{\text{cc}}$...so we assert:
$$\text{density of brain tissue is approximately } 1.0 \frac{\text{g of brain tissue}}{\text{cc of brain tissue}}$$
Accordingly, if we multiply $V_{\tau^*}S\frac{ \text{mol of N2O in brain tissue}}{ \text{cc brain tissue}}$ by the inverse of the brain density, we have:
$$V_{\tau^*}S\cdot 1\frac{ \text{mol of N2O in brain tissue}}{ \text{cc brain tissue}} \cdot \frac{\text{cc of brain tissue}}{\text{g of brain tissue}}=V_{\tau^*}S \frac{\text{mol of N2O in brain tissue}}{\text{g of brain tissue}}$$
Therefore, the more correct way of writing $(\dagger_1)$ is:
$\frac{Q_B(\tau^*)}{W}=V_{\tau^*}S \cdot \rho^{-1}_{\text{brain}} \quad \color{green}{(\dagger_2)}$
At this point, if we substitute the $\color{green}{(\dagger_2)}$ expression in for the CBF formula, we have:
$$\text{CBF}(\tau^*)=\frac{V_{\tau^*}S \cdot \rho^{-1}_{\text{brain}}}{\int_0^{\tau}\left[A(t)-V(t)\right]dt}\left(\frac{\text{cc}}{\text{min}\cdot\text{g}}\right)$$
I suppose as long as you remember what the units are, given that the magnitude of $\rho^{-1}_{\text{brain}}$ is approximately $1.0$, we can drop it from the equation and write:
$$\text{CBF}(\tau^*)=\frac{V_{\tau^*}S}{\int_0^{\tau}\left[A(t)-V(t)\right]dt}\left(\frac{\text{cc}}{\text{min}\cdot\text{g}}\right) \quad (\dagger_3)$$
NOW, to answer the question of where does the $\frac{1}{100 \text{g}}$ come from...honestly, I feel like it is completely arbitrary and have no sense as to why this choice was made. As far as I can tell, Kety & Schmidt could have just as easily left the equation in its $(\dagger_3)$ form. However, for some reason that hopefully someone out there can figure out, they decided to multiply $(\dagger_3)$ by unity in the form of $\frac{100}{100}$, which then allowed them to rewrite $(\dagger_3)$ as:
\begin{align}\text{CBF}(\tau^*)&=\frac{100}{100}\times\frac{V_{\tau^*}S}{\int_0^{\tau}\left[A(t)-V(t)\right]dt}\left(\frac{\text{cc}}{\text{min}\cdot\text{g}}\right)\\&=\frac{100V_{\tau^*}S}{\int_0^{\tau}\left[A(t)-V(t)\right]dt}\left(\frac{\text{cc}}{\text{min}\cdot\text{100 g}}\right)\end{align}

I don't think any of this complication is necessary. There's a tradition in medicine to express in convenient units, where "typical" values are in the range of 10s to 100s, avoiding scales where values right of the decimal are important and values where values left of the decimal are meaningless.

@BryanKrause Well, it at least explains the dimensional mismatch stated in $(\dagger_1)$, so perhaps it is of use to someone. Though that tidbit about medical history is interesting. Thanks~

Oh, I see, I assumed your question was mainly about the "100" rather than the "grams". I think that one is pretty straightforward, too... Blood doesn't go places for fun, it feeds tissue. If you have different sized organs (say, in different individuals) they're going to have different blood flow not because of any sort of pathology or "interesting" difference but just because of the organ size difference. I wouldn't consider that a mismatch in dimensions any more than expressing, say, GDP per capita.

If you're wondering why mass instead of volume, blood is something you can pour into a measuring cylinder because it's liquid. Tissue isn't liquid and you can't easily measure its volume. You could use displacement but then you have to stick it in some other solution in a sufficient container. Easier to put on a scale.


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How does bonding between non-complementary bases occur?
My teacher told me that when DNA polymerase makes an error (roughly every 10 million nucleotides?) that if, for example, it matches an A with a G that the error remains and is the main cause of point mutations. How do the two bases that aren't complementary remain bonded?

How do the two bases that aren't complementary remain bonded?

Non complementary bases can only form non-Watson-Crick bonds, which are very unstable and noticeably different.
Therefore any mismatch in the DNA of the genome will form a recognisable disruption of the DNA helix. This disruption is usually removed very quickly by the cells, since it makes DNA much more unstable.
Most cells have multiple mechanisms to detect and repair these sites, with one system specifically dedicated to DNA mismatch repair.
This system acts on mismatches directly after DNA replication, since at this point specific markers (sometimes DNA methylation, sometimes not fully understood) can differentiate between the newly synthesised DNA strand (which may contain an error) and the old one.
The repair mechanism will remove the mismatch and replace it with a properly bonded base pair, so that mismatches in the DNA are always short term issues - it is still possible though that 'wrong' mismatching base is replaced, which then (finally) leads to a mutation.
The error rate of DNA polymerase (1 in 10^7 sounds about right, this is the combination of the initial error rate and the DNA polymerase proof-reading mechansim) therefore has to multiplied with the error rate of this repair mechansim, which is around 10^3 (I can't find a source for this right now), to get a final error rate of DNA replication in cells.

"They do not" is incorrect. Non complementary base pairs do form, and remain until they are removed. They are less stable, and produce a detectable change in the 3-d structure of the duplex. The rest of your answer is correct.

@DeNovo edited the answer accordingly


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Primitive streak being only present in caudal half of embryo affecting gastrulation?
It is my understanding that in gastrulation epiblast cells migrate to the primitive streak where they start to form the three germ layers; does this mean that gastrulation only occurs at the caudal half of the developing embryo

What organism are you asking about? 2. Where are you getting the idea that the primitive streak is only in the caudal half? 3. What do you understand gastrulation to mean?

Humans. It came up in one of my lecture notes and in my understanding gastrulation is the formation of the three germ layers (ectoderm, mesoderm, endoderm) from the epiblast

It would help a little in answering your question to know more about what organisms you are interested in, or the specific source that you are referencing, with e.g. the relevant quote.
For example, the primitive streak is specific to amniotes: avians, mammals, and reptiles. In other common model organisms such as flies or amphibians gastrulation happens differently.
Another thing to keep in mind is that gastrulation is a very large and structurally distending process, so it can't be really said to happen "only on one end" of the embryo. The whole embryo is going through gastrulation. We can however talk about the placement of certain gross morphological structures on the embryo. But really each cell is affected by gastrulation, whether it's immediately obvious under a microscope or not.
Looking at the Amniote section of the wiki page on gastrulation, it appears that the main morphological changes in gastrulation do occur on the caudal side - for amniotes.
However, in Drosophila, gastrulation involves the formation of an approximately homologous structure called the ventral furrow, which is obviously on the ventral side, extending most of the anterior-posterior axis. However the invagination event does actually happen on the dorsal/caudal side.
So, it's complicated, and it depends a lot on which organism you're talking about.
Update following response
Humans are amniotes, they follow more or less the normal amniote path in gastrulation according to the wiki link above.
An important note missing in my previous answer above is that gastrulation itself defines bilateral symmetry in embryos; prior to this establishment animal-vegetal is the only obvious axis. So we are kind of defining the rostral-caudal axis according to the formation of such structures as the primitive streak, which are formed during gastrulation.
So it's a little circular to say that gastrulation happens on caudal end only; as gastrulation includes the step that establishes the rostral-caudal axis. Without gastrulation that axis just doesn't exist.
Again, gastrulation is a process that happens to the entire embryo. It doesn't just happen in one area. Structures such as the primitive streak are just obvious clues that the process is happening. It might be proper to say that the primitive streak begins forming caudally (I don't know of exceptions, though I'm not an expert), but it would not be proper to say that gastrulation is a caudal process.

Hi thanks for the answer I meant in humans

@FazalSyed see update.

Your point that gastrulation defines the axes is a good one. I would also note that the organizing node and primitive streak are not "in the caudal half" as the OP says. They move, which is a key point. Specifically, they move in a rostrocaudal direction (or craniocaudal if you prefer), the axis is established based on that movement. Early cells that pass through the streak form more rostral structures. Later cells form more caudal structures.

I think the Wikipedia article has confused the OP with poor word choice when it says the primitive streak forms "toward the caudal or posterior end." It doesn't form at the caudal end. It moves towards that end as gastrulation proceeds


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Can the human body store protein?
I am interested to know if a human body can store protein.
Absolutely for the bodybuilders, does it really matter if they divide their protein consumption during the day or eat all of it in one meal at anytime they want?
Is there any constrain on protein absorption per hour?
What will happen for the extra protein we eat?

The human body can not store Proteins (technically).
BACKGROUND :
PROTEIN is a very broad term and there are hundreds and thousands of proteins.[1]
Proteins are heteropolymers consisting of amino acids held by peptide bonds.
Amino acids :
There are 9 amino acids which we need to intake.

Phenylalanine, valine, threonine, tryptophan, methionine, leucine, isoleucine, lysine, and histidine.

Amino acids our bodies can produce:

These five are alanine, aspartic acid, asparagine, glutamic acid and serine.

These amino acids combine in different arrangements to give those thousands of Proteins. This process is carried out by Ribosomes (cook) and mRNA (recipe) inside every* cell.
Protein metabolism in humans :
During human digestion, proteins are broken down in the stomach to smaller polypeptide chains via hydrochloric acid and proteaseactions. This is crucial for the absorption of the essential amino acids that cannot be biosynthesized by the body.
Trypsin and Chymotrypsin as Trypsin and Chymotrypsinogen are the enzymes  necessary.
.
MAIN ANSWER  :
The excess Amino Acids are broken down into Glucose ( carbohydrate like stuff ) and the Nitrogen moiety is converted into Urea / Uric acids. This is then excreted by kidneys.

Amino acids can be broken down into precursors for glycolysis or the Krebs cycle.
Amino acids can also be used as a source of energy, especially in times of starvation. Because the processing of amino acids results in the creation of metabolic intermediates, including pyruvate, acetyl CoA, acetoacyl CoA and so on; amino acids can serve as a source of energy production through the Krebs cycle.

Therefore excess protein is simply used to make energy like carbs and the Nitrogen part is excreted. Now the excretion process can strain the kidneys due to increased work load, and prolonged stress can lead to malfunctions.
Also,
Our body is very concerned with conserving nitrogen levels, since our body can't fix nitrogen gas (N2) into ammonia (NH3). but, we can't just store huge amounts of ammonia because it's toxic. sugars and fats aren't toxic, so we can store them. because of this, our body either quickly utilizes excess ammonia to make nitrogenous compounds like amino acids and nucleotides, or it excretes it via Urea in our urine.
Problem with Protein storage :
If our bodies had to store proteins, it would need several sophisticated mechanisms and specialised storage cells.( Like we have adipose tissues short fats and lipids storage ).
if you examine the structure of amino acids, they are very similar to many of the carbon-hydrogen-oxygen metabolic intermediates. for example, alanine is an amidated pyruvate, glutamine is an amidated alpha-ketoglutarate, etc. many are easy to make, and most don't cost much to do so, so the body would rather use these intermediates to either:

Create acetyl-CoA, NADH, FADH2, and ATP for energy. this would happen during exercise or starvation.

Create glycogen, fatty acids, nucleotides, NADPH, and other metabolic compounds. this would occur after a big meal, during sleep, and when energy is not needed in high amounts. these compounds are very expensive ATP-wise.

So there's no need to store whole Amino Acids because they can be immediately used for whatever the body needs and then remade when necessary.
We do not store amino acids because we don't need to.
Right dose of Proteins :
Research shows:

A total of 80 g of whey protein was ingested in one of the following three conditions: 8 servings of 10 g every 1.5 h; 4 servings of 20 g every 3 h; or 2 servings of 40 g every 6 h. Results showed that MPS was greatest in those who consumed 4 servings of 20 g of protein, suggesting no additional benefit, and actually a lower rise in MPS when consuming the higher dosage (40 g) under the conditions imposed in the study.

Check here for the interesting results ( this is very relevant to your second question )
Therefore distributed intake of right amount of protein is important!
Scientific literatures :
Proteins:
https://en.wikipedia.org/wiki/Protein_(nutrient)
https://en.wikipedia.org/wiki/Amino_acid
Protein Metabolism:
https://opentextbc.ca/anatomyandphysiology/chapter/24-4-protein-metabolism/
Protein intake and storage:
https://newsnetwork.mayoclinic.org/discussion/are-you-getting-too-much-protein/
https://www.self.com/story/what-protein-does-in-your-body

I have written a long answer, do take time to read and understand

I'll add a more straightforward answer than the previous answerer (who was certainly more in-depth and informative than I will be), for the purposes of clarity. I think protein is stored in the body very much functionally, just not in reservoirs of reserve chemical energy such as adipose tissues do with fat.

I am interested to know if a human body can store protein.

The body cannot store dietary protein; it breaks it down into amino acids, which are absorbed and then turned into protein. One cannot repurpose dietary protein without breaking it down into its constituent monomers, the amino acids.
Amino acids are then used in a plethora of ways, the primary of course being protein synthesis (a kind of anabolism, or 'body-building' if you will). Amino acids are strung together to form newly made proteins for the body's needs, and this is a constant process of (re)building in the body. This is why protein intake is essential for survival, given that it's an essential macronutrient.

Does the body store protein in any meaningful way?

Certainly one could argue that you can store protein by making proteins which are long-lived and later available for catabolism, such as those that make up muscles. The muscle tissue can then be used up at a later time if there is need for energy. This is seen with muscle wasting in the elderly or those that are starved. Proteins are a source of gluconeogenic substrates (see this wiki about gluconeogenesis), and thus can be used as a held store of energy. However, please keep in mind that this phenomenon is rather minimal for dietary protein.
(As an aside: notice I am not talking about proteins that are unavailable for breakdown; many proteins are indeed long-lived, such as collagen, but these escape the ability to be re-used. I wouldn't consider this storage, since their function cannot be said to be one of storage.)

Is there any constrain on protein absorption per hour?

Yes, there is a constraint on amino acid (digested protein) absorption per hour by the GI tract. Most dietary amino acids (and some small peptides) are absorbed in the small intestine, though there is evidence the large intestine can also perform this task in humans.

What will happen for the extra protein we eat?

Remaining protein that is not broken down and subsequently absorbed by the intestinal epithelium, will pass through the digestive track and gets pooped out. Along with anything else that the body was unable to digest, such as fibre (like cellulose which makes up much of plant tissue). Not much more to it. Simple!

Additional interesting readings and protein turnover?

A suggested item if you like.

Does it really matter if [people who wish to be bodybuilders] divide their protein consumption during the day or eat all of it in one meal at anytime they want?

It is certainly possible to live on both regimes. This question is unfortunately off-topic for this SE. There are many different philosophies of body-building.


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What does the term "centromere linkage" mean in genetics?
I am currently learning about tetrad/linkage analysis in yeast. I have read two statements similar to this:

If two genes are unlinked, but linked to the centromere the distribution will be 50 parental ditype (PD) and 50% non-parental ditype (NPD).
If two genes are unlinked, and unlinked to the centromere the distribution will be 1:1:4 in PD:NPD:TT

But I don't quite understand what the term linked to centromere means. I understand that two genes can be linked to each other if they are close together on the same chromosome.
So near the centromere no crossing-over occurs, so does "linked to centromere" just mean that there is no recombination taking place, as it is the case with the first statement?


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If dinosaurs could have feathers, would they still be reptiles?
I just finished watching a video where it was mentioned that nowadays birds are dinosaurs and non-avians dinosaurs could have feathers.
I confirmed this from wikipedia:

Birds are highly advanced theropod dinosaurs, characterised
  by feathers, a beak with no teeth, the laying of hard-shelled eggs, a
  high metabolic rate, a four-chambered heart, and a lightweight but
  strong skeleton.

And:

Direct fossil evidence of feathers or feather-like structures has
  been discovered in a diverse array of species in many non-avian
  dinosaur groups, both among saurischians and ornithischians.

And this family tree of reptiles mentions:

Archosauriformes (crocodiles, birds, dinosaurs and extinct relatives)

And later in the Mesozoic era:

The dinosaurs also developed smaller forms, including the feather-bearing smaller theropods.

So, were these non-avian dinosaurs with feathers actually reptiles?

No.  Dinosaurs were never reptiles, they evolved from reptiles.  Nor are birds dinosaurs, they likewise evolved from dinosaurs, just as mammals evolved from reptiles, and all of those evolved from fish.  It all depends on which branch of the tree you look at, and what forks you decide are important.

@jamesqf So in your opinion Wikipedia is wrong (and also the scientists who accepted the possibility that birds are dinosaurs). How would you classify these particular dinosaurs? Can you detail in an answer, possibly with references (through cladistics)?

@jamessqf Birds are reptiles as are dinosaurs.  http://biology.stackexchange.com/questions/17546/were-there-any-flying-dinosaurs

@Kmm thanks for the link! Your answer provides a good explanation :)

"Reptile" is not a clade. It is a paraphyletic group.

@Armfoot: Yes, Wikipedia is sometimes wrong (and not just about this).  Likewise, the scientists who jumped on the "birds are dinosaurs" bandwagon for the sake of publicity are wrong.  As Remi.b says, it's to some extent a question of semantics, but the principle is that we group things that have similar characteristics under names.  Birds have characteristics that dinosaurs don't (adaptations for flight), just as mammals have characteristics (hair, milk glands) that reptiles don't, so we call them by different names.

@kmm birds are not reptiles. Sauropsids other than birds are generally considered as reptiles.

@WYSIWYG No, birds are within the clade Reptilia, and thus are reptiles.

@kmm birds are specifically excluded from reptilia afaik. If they were included reptilia would have been monophyletic. Sauropsida is the clade that contains both reptiles and birds

@kmm: But as a reductio ad absurdum, would not cladistics define all of these - dinosaurs, birds, reptiles, mammals, &c - as just members of the fish clade?

@jamesqf Actually, yes. Successively broader clades are Sauropsida, Amniota, Tetrapoda, Rhipidistia, Sarcopyerygii, Osteichthyes, Ganthostoma, and Chordata to name a few. The closest thing to a "fish" clade is Osteichthyes. Birds only fall within Sauropsida, as they do their more inclusive clades Dinosauria and Reptilia).

reptiles and dinosaurs and birds are a bit like sharks, fish and bony fish in terms of family groupings.

Taxonomy is dynamic, and conforms to new findings. That birds are nested inside therapod dinosaurs renders Dinosauria paraphyletic. The way you fix this error is to include birds as dinosaurs. Same with reptiles. Birds are reptiles or the taxon "Reptilia" needs to be eliminated. Both are solutions.

Source of information on Biology.SE
This answer offers an introduction to phylogeny on the case study of dinosaurs and birds. If you are not at ease with the concept of monophyletic group, you should definitely have started with this introduction.
This post is somewhat related.
Origin of your misunderstanding
The question is all about nomenclature (and a little bit of semantics). One can call reptiles whatever (s)he wants. The question is what do we define as being a reptile? And the answer is that there are two possible definitions, a common "bad" definition (Definition 1) and a phylogenetic-based "good" definition (definition 2). I think your confusion comes from the use of the same term to mean two different (but related) things.
Definition 1: reptiles
In general, when people talk about reptiles, they talk about turtles, Rhynchocephalia, Squamata and Crocodilia. In this sense, the term reptile is NOT a monophyletic group. In other words, all species being called reptiles (according to this definition) do not share a common ancestor who has no other descendants than the species being called reptiles.
Definition 2: Reptilia
There is a defined monophyletic group called Reptilia. Reptilia is a group that contains all Amniota except the Synapsida (mammals and their extinct close relatives). In other words, Reptilia contains all generally called reptiles (as defined above) and all birds as well as all extinct species that are descendent from this same common ancestor.
Exploring the tree of life by yourself
You will find the tree of life on tolweb.org or on onezoom.org (see The best free and most up to date phylogenetic tree on the internet? for more info).
Using tolweb.org: here are the roots of the tree of the Amniota. And you will probably want to search for the Dinosauria (there) and see how closely related they are to the birds but not so much to the turtles.
Addressing your question directly

If dinosaurs could have feathers, would they still be reptiles?

If by reptiles you mean Reptilia, then whether a given dinosaur has feathers, endothermy, or an exoskeleton (!) doesn't change anything to the fact that this dinosaur is a reptile.
If by reptiles you mean turtles, Rhynchocephalia, Squamata and Crocodilia, then whether a given dinosaur has feathers or not doesn't change anything to the fact that this dinosaur is NOT a reptile!
Known Dinosaurs with feathers?
Given that birds are the only animals that have feathers and that birds are dinosaurs, we don't know of any species that has feathers and that is not a dinosaur! However, when we think of dinosaurs, we usually don't think about a pigeon.
Of course, the Archaeopteryx had feathers too. Archaeopteryx is an avian (bird-like) dinosaur.

But even non-avian dinosaurs such as Velociraptor probably had feathers as well. More info about how closely related is Velociraptor to the birds (Aves) there on tolweb.org. You probably remember the so-called Velociraptor from Jurassic Park movie (on the left) but here is what a Velociraptor probably really looked like (on the right).

The "velociraptors" from Jurassic park actually look more like a large Deinonychus without feathers than a Velociraptor (Thank you @Gaurav in the comments). I suspect because they chose Velociraptor because Deinonychus is much harder to pronounce and way less sexy sounding. Like this, tThe movie Jurassic Park deceived an entire generation about what a Velociraptor is! More information about what the species of Dinosaurs the Jurassic Park movie features in the fun video (in French) Le Vélociraptor from Max Bird.
You might want to have a look at the post Were there any flying dinosaurs? that is very related.
At least, all these big and extinct things with scales are dinosaurs, right?
Well.... not exactly. There are species that many would call dinosaurs that are typically not considered as dinosaurs. Have a look at the MinuteEarth video called "What makes a dinosaur?" for more information in this regard.
Fun and instructive videos

Les dinosaures ont disparu ? from Max Bird and Jamy (in french)

Le Vélociraptor from Max Bird (in French)

What makes a dinosaur? from MinuteEarth

What a great answer!

I believe the "velociraptors" from Jurassic Park are really Deinonychus, not Velociraptor (the dinosaur on the right). Great point about them having feathers, though!

You say "Some dinosaurs actually had feathers". I'd go further and say that every taxon that we know of that has or had feathers is a dinosaur.

I meant dinosaur in the common sense and not Dinosauria. In the core of the paragraph I talk about non-avian dinosaur to make the distinction. I'' edit to really clarify my point and to add the idea that we don't know any animal species that has feather but is not a dinosaur Thnks

The first ever feathered dinosaur tail preserved in amber was found fairly recently. See here for the story!!

Feathers are pretty widespread in therapods, therizinosaurids and tyrannosaurids are known ot have feathers. Even ornithischians dinosaurs may have had feathers.

There have been some good answers here, but I think some information could be added.
Willi Hennig introduced modern phylogenetic systematics, which is sometimes conflicting with traditional taxonomy.
Hennig's important insight was that one should only use synapomorphies (shared derived traits) as the evidence for identifying relative recency of common ancestry within and among groups.
However, many groups, reptiles, fish, invertebrates, etc., are based on symplesiomorphies (shared ancestral traits).
The original question posted above can be addressed with the stem-crown group concept.
Considering the relationship of fossil taxa with living ones, we can ask the following question: do all fossil taxa fit into living clades?
Crocodiles and birds are an excellent example to address this question:
From a cladistic perspective, members of each of the two clades have three types of traits: symplesiomorphies (shared ancestral), synapomorphies (shared derived), and autapomorphies (unique traits).
Where would these traits appear on a phylogenetic tree?
Let us have a look at a bird with a very distinctive bill, the Shoebill (Wikipedia):

This can be considered a unique trait, thus an autapomorphy.
The feathers of the shoebill is a trait it shares with other birds, thus a synapomorphy.
While the shoebill's legs is a trait shared with crocodiles (the sister clade of birds) and many other vertebrates and therefore is a symplesiomorphy.
Thus, autapomorphies appear within the clade, synapomorphies are traits primitively shared by all the members of the clade of interest, but not by members of its sister clade. They are shared but relatively new traits: these traits must have appeared further down the clade, but not below the split between the two sister clades.
Symplesiomorphies are traits shared by the sister clade, or even more distant clades. These traits must have appeared deeper down the tree.
Another question: what sort of organism was the last common ancestor of birds and crocodiles? Was it a bird, a crocodile, or neither? What traits would it have?
By definition of our question, these two groups (crocodiles and birds) are both monophyletic, therefore, one did not give rise to the other. It did not have any of the synapomorphies or autapomorphies in either clade, only their shared symplesiomorphies, and therefore did not lie in either modern clade.
By definition, the organisms that make up the lineage of birds, appearing after the split between the clades of crocodiles and birds, but apart from living birds, must be extinct. We call this the stem group of birds.
The last common ancestor of all living birds, plus all its descendants make up the crown-group of birds. The total group of birds is the crown group and stem group together.
Stem and crown groups are hierarchical, and some crown group taxa have gone extinct, for example, the dodo. The dodo, therefore, belongs in the stem group of pigeons and doves.
By definition, all stem groups are paraphyletic, as they give rise to their crown group. All fossils fall into one or another stem group.
The original question can thus be answered appropriately: dinosaurs are stem-birds and belong in the total group of birds.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Oakland California spider in home
Found this critter this morning on a stack of clothes.  About the diameter of a penny and in my haste to rehome it, took only this photo.  The belly was golden brown.


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What does myelin insulate against, exactly?
I am aware of the saltatory conduction model, nodes of Ranvier and all that, and that myelin lets electrical signals "jump". What does not add up to me entirely is what the myelin sheath insulates against, why it improves conduction through axon. If the cell membrane is already impermeable to ions, why does a "thicker membrane" improve signal conduction? There are nearly infinite memes on the internet about action potentials through axons, have not really seen any answer this though. Some vaguely mention "less leakage", but isn't the cell membrane preventing that to begin with?

Here's an answer I think is fit to answer your question. It gives you a better conception of how myelin does its job of insulation.

Ions have an electrical charge which generates an electrical field that decreases in strength with distance from the ion. The cell membrane of the axon is not thick enough to stop ions on either side from being attracted to one another and interacting. The electric fields of these ions are what myelin 'insulates against'. This answer to a related question provides some good diagrams and in-depth discussion of how increasing the distance between the oppositely charged ions helps nerve function.

@Hodgkin Can you look at the two related questions linked in comments by S Pr and timeskull? I think your question should be closed as a duplicate of one or the other.

So, myelin increases the distance to the positive ions on the outside of the axon membrane, preventing them from repelling the positive sodium ions that travel down the internodal segment by electrotonic conduction, overall decreasing resistance to sodium ion current?

If that is the answer, then technically it isn't really insulating (as insulation does not insulate against electric fields?), but, just increasing distance (with non-charged matter, the myelin)? insulation in wires prevents leakage of electrons, doesn't it? isn't the metaphor, if so, misleading?

A capacitor involves plates holding charge separated by an insulator - adding more insulator increases the separation. Adding a non-insulator would not. There is also increased resistance overall. So no, I don't think it's misleading nor an analogy, though it's important to realize that biological electrical systems only approximate the perfect/ideal mathematical circuit components (even more so than non-biological versions).

I don't think your statement about positive ions repulsing is correct, either. Just think about it as the amount of charge necessary to change the membrane voltage is less.

The dielectric in a capacitor is insulating, good point. If not by decreased repulsion from the positively charged ions on the other side of the myelin dielectric, then how does the decreased capacitance in the internodal segment improve propagation of the sodium ions?

(what I meant with misleading, it seems to me that insulation around a copper wire is used to prevent leakage, not to decrease capacitance, since the space around the wire isn't electrically charged whereas extracellular space is. better to liken it to a capacitor then, like you did. I got that analogy, which was not an analogy because it is what it is, but maybe you get what I mean)


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Are mosquitoes attracted to blue lights in particular?
I've been confronting the fact since childhood that mosquitoes are attracted to lights, especially blue lights. Now I know that all insects including mosquitoes are attracted to bright light but I never got it verified that if they are specially attracted to blue light or not. Is it true or just another urban myth?

It is not an urban myth. UV and blue lamps are good insect attractants. They have been used for many decades in insect traps, and these too work for mosquitoes. These lamps are routinely used in ecology at insect sampling sites. In some cases, such as with diurnal moths, yellow lamps can also be good attractants. The reason why UV is applicable is because insects are equipped with three photoreceptors, namely the UV-, blue-, and green-sensitive photoreceptors. Below you can see the spectral sensitivity curves of the genus Apis, which is typical for many insects.

As to why they are good attractants is probably variable across species, because it would depend on the neurological encoding of this information. For instance, some species may use this information to determine night and day, or may be superstimuli for nectar as used by plants to advertise themselves for pollination. Or it may simply be for some other reason.

Nice answer. +1. However, it could address the OP's question about mosquitoes more directly. I'd suggest updating with some specific evidence about mosquitoes if you can find something.


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How does non-cell autonomous work - how can a mutant cell make other non-mutant cells exhibit a mutant phenotype?
I am reading a journal paper, and I have coming across the following statement:

Furthermore, although late-born neurons that take up exogenous Dcc
fail to settle in the superficial layer of the dorsal horn, other
non-electroporated late-born neurons exhibit no apparent aberrant
migration. Thus, Dcc appears to function in a cell autonomous manner.

I am not sure, in the context of the paper, what is meant by "cell autonomous". I have come across this definition, where it is said that cell autonomous means: "A genetic trait in multicellular organisms in which only genotypically mutant cells exhibit the mutant phenotype. Conversely, a nonautonomous trait is one in which genotypically mutant cells cause other cells (regardless of their genotype) to exhibit a mutant phenotype."
I am assuming that cell autonomous in the context of this paper is that neurons that took up exogenous Dcc had migration defects, while neurons that didn't take exogenous Dcc migrated properly.
One thing that I am wondering is, in the context of non-cell autonomous, how can a mutant cell make other non-mutant cells exhibit a mutant phenotype? Any insights are appreciated.

This is one of those cases of biology terminology that really makes me groan, because although it can be a useful designation, the word choice is just... not excellent.
Cells interact with each other all the time, particularly in a multicellular organism: it's absolutely essential that they do. That means that one cell type can influence the behavior of another cell type.
When you describe some mutation as "cell-autonomous", you're basically saying that the phenotype is just dependent on the cell where the mutation is expressed. For an example off the top of my head, a mutation in a pigment-producing enzyme causing albinism is almost certainly going to be cell-autonomous: if you introduced the mutation in only the pigment-producing cells, you'd get exactly the same result as if the entire organism had the mutation. You could understand what is going on if you just cultured some of those cells in a dish and compared those with and without the mutation. You don't need the whole organism to understand what's going on, just the autonomous cells in a dish.
You ask about non-autonomous, though. Again, I think it's easier to use some example. Searching Google scholar for "non cell autonomous" one of the first results is this paper:
Di Giorgio, F. P., Carrasco, M. A., Siao, M. C., Maniatis, T., & Eggan, K. (2007). Non–cell autonomous effect of glia on motor neurons in an embryonic stem cell–based ALS model. Nature neuroscience, 10(5), 608-614.
They're looking at mechanisms of amyotrophic lateral sclerosis (ALS). ALS is a neurodegenerative disorder: the overall phenotype is that neurons die. However, this paper isn't about neurons, it's about glia. When you co-culture neurons and glia, you're looking at the neurons for the phenotype (do the neurons die?), but it's the glia where the genetic manipulation matters. This particular paper is about SOD1, which is involved in protection from oxidative stress.
Back to your paper, this is talking about neuronal guidance cues that are important in the developing nervous system. Simplifying a bit, typically neurons express some collection of receptors for various guidance cues, and other cell types present these cues on their cell surface or excrete soluble molecules. Growing neurites then follow the concentration gradients (either in an attractant or repellant fashion) to get where they belong. Dcc is also called the netrin receptor. The authors describe mutations in Dcc as being cell autonomous for neuronal migration, because you only need the mutation in the neurons to see the phenotype. This makes sense mechanistically because it's a receptor expressed by the neurons themselves.
However, if you had a gene of interest involved in netrin-1 synthesis or expression, that would possibly demonstrate a cell non-autonomous phenotype: it doesn't matter if you interfere with netrin-1 expression in the neurons themselves; as long as their receptor and signaling pathway is intact, they'll navigate just fine. However, if you put normal, unmutated neurons into a nervous system where all the other cells fail to express netrin-1, even those wild-type neurons won't know where to go. The phenotype: failed migration, is occurring in a different cell type than the ones that need to be genetically altered for the organism to show the phenotype.


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Cell Signaling: What is meant by "sustained tonal induction"?
I am reading a journal paper about the insulin-like growth factor 1 receptor. I have a question about the following statement in the paper:

IGF/IGF-IR stimulates the PI3K-Akt pathway in a stereotypical way –
sustained tonal induction. Sustained induction is thought to define
the specific biological outcomes of IGF signaling, and distinguish the
function of the IGF ligand from other RTKs/ligands that access the Akt
cascade (Gross and Rotwein, 2016; Kubota et al., 2012). In particular,
sustained activation of the PI3K-Akt pathway, mediated by IGF-IR,
induces cell proliferation in multiple types of cells, cell survival
in neural cells, and protein homeostasis in skeletal muscle cells
(Fernandez and Torres-Alemán, 2012; Fukushima et al., 2012; Ness and
Wood, 2002; Sacheck et al., 2004; Stewart and Rotwein, 1996). To date,
the mechanism by which IGF-IR produces sustained signaling remains
poorly understood.

What is meant by "sustained tonal induction"? I have searched online but could not find any specific results.
Any advice is greatly appreciated.

On a quick (limited) search, it looks like that's the only paper using that particular phrase, but the concept of sustained activity is explained in the body of the paper. I'd throw out the tonal; sustained induction of that pathway is discussed in many papers.


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Why do receptor tyrosine kinases undergo constitutive endocytosis?
I am reading a journal paper about the endocytosis of receptor tyrosine kinases. I have a question about the following statement:

At the cell surface RTKs undergo constitutive endocytosis
(internalization) at a rate similar to that of other integral membrane
proteins. Constitutive internalization of RTKs is much slower than
their constitutive recycling from endosomes back to the cell surface.
Therefore, RTKs are accumulated at the cell surface, which allows
maximal accessibility to extracellular ligands.

I know that RTKs get endocytosed upon binding of their ligand and either get targeted for lysosomal degradation or get recycled back to the cell surface. Lysosomal degradation of the receptor is a mechanism to downregulate levels of the receptor and control the strength/duration of the signaling.
However, what is the purpose of constitutive endocytosis of RTKs? Further, does this occur even if the ligand is not bound to the receptor?


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Role of Prevalence in Estimating Coronavirus Mortality
Let there be a sample of 10,000 people.
100 of them have a fever. You test them for COVID19 and they all come out positive.
5 of them die, 9 of them end up in intensive care.
The estimated mortality is 5%, and estimated intensive care rate is 9%.
What about the 9,900 asymptomatic people who did no get tested?
Scenario A: All 9,900 asymptomatic people would test negative for COVID19.
Scenario B: All 9,900 asymptomatic people would test positive for COVID19 because of a combination of high rate of asymptomatic carriers and high false positive rate.
End result:
Scenario A: true mortality rate is 5% and true intensive care rate is 9%.
Scenario B: true mortality rate is 0.05% and true intensive care rate is 0.09%.
the numbers are fictitious, but the point is simple - we can't estimate mortality without knowing the prevalence
Question:
Where are we right now between scenario A and scenario B? Or put another way, are there any ongoing studies/reports which take into account this factor?

Update, using real numbers:
Italy has a 250 cases/1mil pop (0.025% of the population tested positive)
That’s 15k cases, and 1k deaths (7%).
Scenario A - the remaining 99.975% are 100% Covid-free:
Mortality is 7%.
=> If 100% of the planet is infected, 490mil die.
Scenario B - the remaining 99.975% are asymptomatic, but positive Covids:
Mortality rate is 0.0001%.
=> If 100% of the planet is infected, 7k die.

I think you're talking (setting aside false-positive/low-specificity testing problems for the moment) about the difference between infection fatality ratio (IFR, fraction of infected people who die from disease) and the case fatality ratio (CFR, fraction of clinically defined "cases" who die from disease). The difference between these two depends completely, as you suggest, on the difference between the population that gets infected and the population that is defined as a "case" (which could vary a lot: is it people who have a cough? fever & cough? request testing? are admitted to the hospital? are admitted to the ICU?).
Because most of the people aboard the Diamond Princess cruise ship were tested (3063/3711), we can have a reasonably good idea of the fraction infected (unlike the usual scenario where most asymptomatic cases are never noticed). The authors of this (not yet peer-reviewed) study concluded that:

the all-age cIFR on the Diamond Princess was 1.2% (0.38–2.7%) and the cCFR was 2.3% (0.75–5.3%)

(where 'c' in cIFR and cCFR stands for 'corrected'; these are estimates that account for the fact that we don't yet know the outcome for all patients).
Other issues to think about:

sensitivity and specificity of testing (false positive/negative rates)
variation with/adjustment for age (discussed in the paper)
variation by medical/social context (e.g. Wuhan vs Iran vs places where cases are caught early and the medical infrastructure isn't overwhelmed)

Russell et al., "Estimating the infection and case fatality ratio for COVID-19 using age-adjusted data from the outbreak on the Diamond Princess cruise ship". https://cmmid.github.io/topics/covid19/severity/diamond_cruise_cfr_estimates.html

Comments are not for extended discussion; this conversation has been moved to chat.


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How can I classify the 3 clades(S, G, V) of the coronavirus that are found on GISAID?
On GISAID they classified the corona using 4 clades(S, G, V, Other).
I would like to know exactly how these genomes were classified for my research.
So how do you classify a coronavirus genome as belonging to one of the clades.

is there something in your question that is not answered on the GISAID website? e.g. https://www.gisaid.org/references/statements-clarifications/clade-and-lineage-nomenclature-aids-in-genomic-epidemiology-of-active-hcov-19-viruses/#:~:text=Clade%20and%20lineage%20nomenclature%2C%20July%204%2C%202020&text=GISAID%20clades%20are%20augmented%20with,pandemic%20strain%20causing%20COVID%2D19.

*The question is a duplicate of this one.
There are many techniques, all encompassed in what is known as molecular phylogenetics. To get 'clades' or any other groups, you need the sequences of your organism (a virus, in this case, each sample will have its own sequence), and then you need to align these sequences (to match the regions that can be compared, remove 'blanks', 'duplicates', etc). The alignments will differ in some informative positions, and these differences will give you an estimate of how close are some sequences to others, forming groups (or 'clades' in technical terms). So, how do you actually do this? I don't think Stack Exchange is the proper forum for this if you are doing scientific research (I'd recommend you talk to your advisor or a colleague). But if your research is just for curiosity and you need some basic place to start, I'd recommend you to check out MEGA, and this paper. There they explain, step by step, how would you go about this.
And where do you get the sequences? Well, if you are looking at a specific paper they usually give you the 'accession number' of the sequence(s) they are reporting, and if you just want to find your own sequences for your own study, you can search the GeneBank.

Thanks for the answer. I already have the genomes and I already have done many alignments in the past so this is not new for me. What I need to know is how to exactly classify a coronavirus genome as belonging to one of the clades mentioned in the question. I asked a similar question before and got a very appropriate answer. This is the kind of answer i'm looking for(In the link).
https://biology.stackexchange.com/a/90896/57497

If this is for serious research I'm sure you have people who could really help you in your university/department, and not a random stranger in Stack Exchange. However, I noted that the answer you are looking for is already in the top left corner of your image. The criterion the authors of the study used is there in plain sight. Good luck!

The clades have an origin point from which they can see changes in the virus structure to define the clades themselves. The origin point, or reference is the established SARS-CoV-2 reference genome, NC_045512. The clades are mainly named after the mutations that amino acids and proteins have had.
Source: https://www.who.int/bulletin/volumes/98/7/20-253591/en/
They look for different types of mutations and what variants in the SARS-CoV-2 lead to these. Sequences are submitted from across the globe and uploaded to GISAID and analyzed. For example, the S and L variants. There's been a change in the amino acid leucine to serine. So the clade encompasses both but the change to serine (S) defines the clade.
For ORF8-L84S (as seen in picture), the ORF8 gene underwent a mutation of the amino acid L at the 84th position of the gene’s protein to the amino acid S. In other clades, such as G changes aspartic acid at position 614 to glycine. Clade V is labelled NS3-G251V, where the NS3 gene’s glycine at position 251 changed to valine.
So for the naming in general it goes like this:
Clade S - ORF8-L84S
ORF8 (gene undergoing mutation)
L84 (L indicates amino acid leucine at position 84)
S (last letter indicates what it changed into, and defines the clade)
Here's a picture of the SARS-CoV-2 encoding sequence structure and location of common mutations:
Source: https://www.biorxiv.org/content/10.1101/2020.05.03.066266v1.full
The mutations define the clades. You collect the sequences and run a maximum likelihood (ML) phylogenetic. This will show you how the sequences are clustered compared to your reference genome. You can then do a lineage classification software (Pangolin COVID-19
Lineage Assigner).
So for classifying the clades they align the struces with reference genome NC_045512. They look for changes or mutations in the virus and separate them into clades. This might also be done by functional and non-functional mutations but I am not sure if that is included into GISAID.


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Where can I find the genome of the L-strain coronavirus and the S-strain coronavirus?
I read an interesting article about two strains of the coronavirus:
https://www.newscientist.com/article/2236544-coronavirus-are-there-two-strains-and-is-one-more-deadly/
I would like to know how the scientists used to classify a coronavirus as l-strain and s-strain.
And more specifically I would like to have the genome(The DNA) for a l-strain and a s-strain.

“Two of the key claims made by this paper appear to have been reached by misunderstanding and over-interpretation of the SARS-CoV-2 data, with an additional analysis suffering from methodological limitations ... Given these flaws, we believe that Tang et al. should retract their paper, as the claims made in it are clearly unfounded and risk spreading dangerous misinformation at a crucial time in the outbreak." —Response to “On the origin and continuing evolution of SARS-CoV-2”

Article links to this publication which has all the information needed:
https://academic.oup.com/nsr/advance-article/doi/10.1093/nsr/nwaa036/5775463
It is mentioned in the paper that:

Although we found only 4% variability in genomic nucleotides between
  SARS-CoV-2 and a bat SARS-related coronavirus (SARSr-CoV; RaTG13), the
  difference at neutral sites was 17%, suggesting the divergence between
  the two viruses is much larger than previously estimated.

Their results highlight evolutionary changes in the development of new variations in functional sites in the receptor-binding domain (RBD). These developmental variations have a spike in changes to the RBD of SARS-CoV-2 and viruses from pangolin SARSr-CoVs
How do they define S and L variations?
They did population genetics on 103 available SARS-CoV-2 genomes.
These two major types are well defined by two SNPs which show complete linkage across the viral strains.
It also important to mention that SARS-CoV-2 was found to have 96.2% similairty to a bat SARS-related coronavirus (SARSr-CoV; RaTG13) but not very similar to SARS-CoV (79%) or MERS-CoV (50%).
How do we know that there's two type?
We know there's two types because from the 103 sequenced genomes two SNP locations show significant linkage. These are SNPs at location 8,782 (orf1ab: T8517C, synoniumous) and 28,144 (ORF8: C251T, S84L).
If you have a "CT" (as in base pairs) haplotype SARS-CoV-2 you've got the L-type ("L" type because T28,144 is in the codon of Leucine). Otherwise, if you've got a "TC" haplotype you have the S-type (C28,144 is in the codon of Serine).
They found that S-type is the ancient (less aggressive version) by aligning it with other older viruses. In fact for each variant of the virus the ancestral state was inferred by alignments of SARS-CoV-2 (NC_045512), RaTG13, and GD Pangolin-Cov.
So to be more precise on my answer for finding S and L types. You sequence the genome of an infected individual (you can find these online on NCBI) align it with the current reference sequence (MN908947, NC_045512), look at the SNPs and figure if they have a "CT" or "TC" haplotype to determine S or L type.

I downloaded the complete genome of MN908947 and NC_045512.
They are both identitical.
Aren't they supposed to be different?

The paper was a little confusing on that. I aligned them and you're right. I changed my answer to reflect your question better.

I downvoted this answer because it doesn’t point out that the notion of two biologically significant strains is nonsense, the product of incompetent researchers messing with things they don’t understand. See genuine experts’ opinion in Response to “On the origin and continuing evolution of SARS-CoV-2”

Understandable, I'll read the linked page and see if I can add more clarity to the answer with more correct research. Feel free to edit/modify my response or add a new one.

Hey you were really useful in answering this question. Could you help me with another similar question? I would really appreciate it!
https://biology.stackexchange.com/questions/92383/how-can-i-classify-the-3-cladess-g-v-of-the-coronavirus-that-are-found-on-gi

I know it's been a while, but in case anyone comes back to this: since the beginning of the pandemic, many tools have been developed to help identifying lineages and clades.
L-Strain corresponds to Pango lineage B and descendants including all VOCs like Alpha, Delta and Omicron.
S-Strain corresponds to Pango lineage A and descendants (and Nextstrain clade 19B).
To find out if something is A/B, just drop them into Nextclade and check the Clade column. Everything is L, unless it says 19B:

In this example, the sequences with id #2, #3, and #4 are S, everything else shown is L.
Disclosure: I'm a Nextstrain/Nextclade developer.


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Why don't breast enlargements leave any marks of surgery on breasts?
If we get stitches, we get marks left on the skin, but there are no marks for breast enlargements. I saw a YouTube video about a breast enlargement wherein a doctor makes a cut. Where does the cut mark go after surgery?

All cuts that go through the dermis (the full thickness of skin) will leave a scar, no matter what (and no matter what anyone tells you). The visibility of scar tissue has a lot to do with how a person heals, how much stress is put on the incision as it's healing, where the scar is, if it crosses the natural direction of skin (called Langer's lines) or goes along the lines.
Plastic surgeons have many years of training and experience in cosmetic skin surgery, and know how to minimize scar formation by their more fastidious closure methods and wound care, as well as hiding scars in ceases and along Langer's lines. But even the best plastic surgeons cannot prevent scars, only minimize them. If you still don't believe breast augmentation doesn't leave scars, you can look at this page (NSFW).

They don't always cut through the breast.  The armpit is a common alternative to slicing the breast tissue.  In these cases, there is absolutely no scarring on the breast of any kind.

authors: سید عباس حسینی تلگردی


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Doubling the concentration of extracellular calcium hyperpolarizes a neuron. Why?
I was doing some back of the envelope calculations to try to answer this question in more mathematical terms. Essentially the question states: Why does increasing the extracellular potassium concentration depolarize a neuron, while increasing the extracellular calcium concentration hyperpolarize the neuron?
My initial thought was that there is a change in the equilibrium potential for each ion. Working this out however I realized I was wrong in my reasoning; my math proved me wrong.
Doubling the concentration of extracellular potassium makes the equilibrium potential of potassium 17.8 mV more positive. For calcium, it increases the driving force by 8.9 mV (based on room 300 K temperature). What this means to me is that both will cause the resting potential of the neuron to become slightly more positive, though calcium less so.
This is indeed obvious: adding more positive ions to the outside of the cell increases the driving force for that ion, and assuming there is any conductance (albeit small) then there will be some depolarization of the neuron.
This makes me think that this is not a phenomena explained by a neuron at rest. Some other mechanism is responsible for increased extracellular calcium causing the neuron to hyperpolarize.
My possible guesses:

If the calcium concentration is doubled, then the driving force for calcium increases, so there is more influx of calcium and thus the internal calcium concentration will increase. Because the concentration of calcium ions on the inside was previously near zero, now that internal concentration will rise to be some significant number, thereby hyperpolarizing the neuron.
The internal concentration of calcium rises slightly, but instead of (or perhaps in conjunction with) lowering the resting potential directly, there is more activation of calcium-activated potassium channels, thus raising the conductance of potassium ions, and thus ultimately hyperpolarizing the neuron.

Am I on the right track or am I missing something?

I edited this to clean up some of the misuses of terminology. One quick suggestion: the names of these ions are not capitalized ("Potassium", etc.). In fact, more often you will just see K+, Ca++, Na+, and Cl-, which is more convenient to write. Also, there is no such thing as the resting potential for an ion, just for the whole neuron; for the ion, it is the equilibrium potential or reversal potential. Etc.

"This makes me think that this is not a phenomena explained by a neuron at rest." Why not? If the neuron is not spiking--which it is not in your example--it is at rest.

This paper and this paper supports the second possibility I hypothesized. That is a increase in external Calcium concentration leads to an increase in conductance of Potassium.
While the increasing the external Potassium concentration can be shown to depolarize the cell with by calculating the Nernst potential for the Ion, the Calcium Ion has a non-intuitive effect. This means if one increases the outside concentration of Calcium Ions then inevitably there will be a small increase in the internal concentration of Calcium ions on the inside. This will slightly bias the Calcium Activated Potassium Ions to be a little more open. Thus raising the conductance of Potassium. This will mean there is a net hyperpolarizing current keeping the cell less excitable.


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Is there selection against long proteins and long genes?
Background thought
Titin and TTN
Titin is the largest protein in the human genome with 33423 amino acids. Titin is coded by the gene TTN that must be at least $3 \cdot 33423 \approx 100kb$ long. Looking at NCBI entry for the gene TTN indicate that TTN is actually about 240kb long.
Transcription rate
The average transcription rate (Ref.) is around 1.5kb per minute. It therefore takes about $\frac{240k}{1.5k * 60}$ 2.5 hours to transcribe TTN in mRNA. This mRNA then need to be spliced before being available for being translated. Per consequence, I don't think it is possible for translation to happen in the same time as transcription but might well be wrong.
Translation rate
The translation rate is about 8.4 amino acids per second (Ref.). It therefore takes about $\frac{ 33423} { 8.4 \cdot 3600}  \approx 1$ hour to translate the protein. Sure, several ribosome can translate the mRNA in the same time but it still remain that it takes 1 hour to synthesize at least one protein.
Transcription + Translation rate
Assuming translation does not occur in the same time as transcription, the total time to create the first protein of titin is about 3.5 hours.
Half-life
The half-life of a typical human protein is 6.9 hours (Ref.). Intuitively I would expect a negative correlation between mRNA size and mRNA half-life.
Half-life and Transcription + Translation rate
Because the time to produce the first protein is about half the half life, it means that a quarter of every single mRNA that is being produced would never give rise to even a single protein because it would degrade before either before or after translation has started.
It sounds like an important cost and would be surprised if a gene or a protein could be any longer.
Question
Is there evidence of selection against long proteins and long genes?
Are there proteins that are much longer than Titin in other species?
Do I exaggerate the cost it represents, either by not considering that an average rate (such as transcription rate) is not representative of the actual rate for typically long gene/protein or by assuming that it is costly to create tons of mRNAs that won't never be translated?

You are forgetting that there would be a lot of ribosomes on a single mRNA.  Also, there could be multiple RNA polymerases transcribing the gene.

Sure. It still remain that it take 3.5 hours to synthetize the very first protein and I'd expect it to fail 25% of the time.

Let's say it does take 3.5 h to make a single protein from the point when transcription is initiated. However, titin is a structural protein and is not some kind of protein that has to quickly respond to stimuli. Once the protein reaches steady state then it is just continuously made. Imagine a transcription event that started at time t which culminates in the protein production at t+3.5h. Let's say there is another transcription event that started at t+0.1h which will end up making protein at t+3.6h. You are getting a protein molecule at every 0.1h. Do you get my point?

Similarly, there are multiple ribosomes on the mRNA. If it takes 1h for a single ribosome to traverse through the ORF and let's say there are multiple ribosomes on the mRNA placed 0.1h away (convert that to #codons), you'll end up getting a protein molecule from a mRNA molecule every 0.1h.

I think I get this point. I understand that it is feasible to produce proteins at a constant desired rate. It still remain that plenty of mRNA will degrade without being of any use and that plenty of mRNA will degrade during the translation, leaving half synthesize protein that are of no use either. All of this represent a cost that is much more important for a long gene and long protein than for a short gene and short protein. Thanks for your help!

The mRNAs can be quite stable.

Is there evidence of selection against long proteins and long genes?

I am not aware of any such evidence and cursory googling did not reveal studies that researched a correlation between gene selection and gene size. However,  the larger a gene, the larger the probability of a deleterious mutation within said gene so I expect that there is some limit to the size genes can reach and be stable through evolution.

Are there proteins that are much longer than Titin in other species?

To date, titin is the largest known protein

Do I exaggerate the cost it represents, either by not considering that
  an average rate (such as transcription rate) is not representative of
  the actual rate for typically long gene/protein or by assuming that it
  is costly to create tons of mRNAs that won't never be translated?

I really like how you estimated the time cost of producing titin. However, as you already suspect, I believe that you have several flaws in your assumptions.
First of all, the stability of mRNA and proteins varies a lot and depends strongly on their sequences. The half life of proteins can vary from minutes to Years. The Titin protein has a half life of ~70 h.
Similarly, mRNA stability varies from minutes to > 12h. Especially household and structural genes were identified to have mRNAs with long half lifes.
Both protein and mRNA stability is not simply governed by random decay but rather by tightly regulated degradation. For proteins, an example is ubiquitinylation which is a process where certain amino acid sequences are recognized and cause the protein to be ubiquitinylated which in turn triggers the degradation via the proteasome. For mRNA, the secondary structure is crucial since certain loop structures can be recognized by RNAses. Thus average protein/mRNA lifetimes do not help to estimate the actual turnover of a specific protein.

+1 Thanks for your answer, that was very helpful. In addition to confirming what I suspected might go wrong with my quick estiamtions, I especially realized that a random negative exponential decay is not a good model for mRNA decay. I appreciate that you make reference to the mutation (which is of $e^{-uL}$, where $u$ is the mutation rate per base-pair and $L$ the size of a gene in infinite population) as it is likely a much more important factor that the one I brought about in my quick estimations. Thanks

I'd expect that genes with the larger probability of a deleterious mutation would be under the stronger evolutionary pressure. Paper http://genome.cshlp.org/content/24/9/1497.full states that "Longer genes are less likely to produce duplicates and more likely to exhibit alternative splicing".

Related to your questions: one thing that is known is that older genes, meaning genes that appear earlier in evolution are longer than new genes. Also new genes evolve faster than old ones.
So new genes are usually short and tend to get larger with time.
Inverse Relationship Between Evolutionary Rate and Age of Mammalian Genes


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How do substances for gene expression work?
How does amplification of gene expression work?
I often find in various articles expressions like "Using substance X or peptide X, we enhanced the expression of gene Z, which led to a certain therapeutic effect.
How to find out which substance enhances the expression of a particular gene? Is there a law, a pattern for this, or, if all this is found out empirically, a summary table of expressing substances?

Try being more specific; Gene regulation is a very broad topic, with lots of intricate mechanisms. Where did you here this? What substances did they use, and for which gene?


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How does the immune system distinguish between a TH1 and a TH2 response?
Hello and thanks for taking the time to read my post.
I know that naive T-Cells (T0) can be induced to become mature T-Helper cells (TH1 or TH2)
by induction with either IL2 or IL4.
IL2+  TH0 -> TH1   Humoral (antibody-mediated)
IL4+  TH0 -> TH2   Cell Mediated response
But what I would like to know is the causal chain that creates the IL2 and IL4 cytokines.
The reason I ask is because one clinician has reported that Azythromycin(an anti biotic) is useful in treating COVID-19(a virus) disease and was wondering if the immune system might become confused about whether should develop a TH1 or TH2 response.
If you can provide me with any help I would greatly appreciate it
Thanks in Advance
Michael Mckeon

From what I have read, the Stage 3 differentiation depends on the surrounding cytokine environment. IL-2 does not specifically promote T-Cell differentiation, it is a general growth factor which promotes proliferation, and is secreted by both profiles.
Differentiation of T-Cell into Th1 is controlled by Interferon Gamma, the production of which is stimulated by IL-12, which is secreted by many APCs (upon stimulation by IFN Gamma produced by cells, in a self-feeding loop). IFN Gamma also suppresses IL-4 production.
Th2 cells are promoted by IL-4. It is not exactly known which cell initially produces IL-4, but it could be basophils. IL-4 then acts in a self-promoting loop, which encourages T-Cells to produce IL-4 as well as other effector cytokines, and also stimulates IL-10 production, which suppresses production of IFN Gamma and IL-12.
Thus, each pathway is self-promoting and suppresses the other pathway, ensuring that the immune response is set in stone.


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What are these two nerves running parallel to the spine called?
I was looking for a human body nervous system, and often times i found a picture like the one below, where there are two nerves running parallel to the spinal column. I searched for it, but nothing came up.

Can anyone tell me what are the names to these two nerve column parallel to the spine and what are their functions?

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


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Is there a known mutation of an insertion type that prevents being infected by a virus?
Recently there was big news about the mutation CCR5 delta 32, that prevents HIV from infecting white blood cells, that was a deletion type of a mutation.
Do we know of an insertion type of mutation that have similar affect? i.e prevents being infected by specific/some virus(s)

Not an insertion but a gain-of-function mutation which causes virus resistance: https://www.ncbi.nlm.nih.gov/pubmed/16306606 Are you looking for human examples or mutations in any organism?

I am happy with any organism


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Is there any explaination to homeopathies in modern biology sciences?
I'd like to know if there is any sort of explaination from rigurous biological arguments which could potentially explain how homeopathies could work?
I'm not talking about placebo effects (psychological) or "water memory" (purely hypothetic), but really about the immune system itself.
Usually, there is only 1, or a really insignifiant amount of toxins after the dillutions for the homeopathies.
But does that mean that there is absolutely no effect on the organism, biologically talking?
Or could there be some immune memory taking place here for example (ik it is usually in adaptative reaction with the lymphocytes, but does it happen with the white cells or other stuff)?
I'm just curious about it :), thanks!

I searched for duplicates on my internet browser but not on stack exchange itself. Sorry for the duplicate, i'll try to be more aware, and thanks.


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What are the different types of SNPs?
When I search for this online I get answers such as substitutions, deletions, insertions etc. But I mean in the sense that I have been reading different terms infront of the word SNP such as: lead SNP, tag SNP, sentinel SNP, indirect SNP, direct SNP, secondary SNP, imputed SNP etc.
From my understanding lead/tag/sentinel are all the same (SNP with lowest P value in a locus, representing the variance in that section). An indirect SNP is also a lead/tag/sentinel SNP and indirect because these have not been genotyped but are in LD with the genotyped SNP + having that they have the lowest P value. Also a secondary SNP is a indepedently correlating SNP, and is specifically independent from the tag SNP? Is there a resource defining these sort of categories? Apologies if this is misinformed, I have been trying to learn about GWAS from different studies, and would appreciate any help to clarify this.

see https://biology.stackexchange.com/questions/73617/gwas-terminology-tag-vs-lead-vs-index-snp

Thank you for this, the paper in the answer was great for the lead SNP definition, although I am still a bit stuck especially with understanding secondary SNPs.


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Determination of a chemical compound in a non-homogeneous sample
This is a more generalized question of my other question here.
I want to know if it is possible to determine a chemical compound in a non-homogeneous sample. I am asking this because we are aiming to create a device that will detect histamine level in fish without homogenizing the samples. In all the journals we've read (which are a lot), fish samples are homogenized (blended + chemically-treated) before histamine is determined.
I am a computer engineering student with basic knowledge on biochemistry. I'm researching on this because this is our thesis topic (which our adviser has forced recommended to us).
Any help/recommendation regarding this is appreciated. Thank you!

You should not actually homogenize samples because histamine works locally. If you know which region is releasing histamine then you can just study those regions. You can actually create a transgenic fish with GFP that is a target of histamine receptor signaling.
Using mathematical models or statistical correlations you can obtain the level of histamine based on fluorescence.
Activated histamine receptor H1 causes production of inositol triphosphate (IP3) which in turn causes release of calcium form ER. You can use Cameleon-GFP to sense the change in calcium levels. However, there are many events that may result in calcium release; you should carefully design your experiment.
This is another possibility (just a guess)- a FRET based study using GFP-YFP FRET Pairs (or other variants). Since histamine receptors are G-protein coupled receptors you may fuse the GFP to alpha subunit and YFP to beta subunit. When upon signaling, the subunits dissociate, you would see a decrease in FRET.

It is correct that imaging-based studies are super-awesome, but question seems to be about chemical. I don't know if there are antibodies available for histamine, if yes, then you can fix and label all sites of histamine.
But imaging through fish tissues (say, more than 1 mm) is close to impossible with molecular resolution and sensitivity.
My best guess would be following. If you are OK with blood level measurements, then try spectroscopic approach. That is measure Raman NIR scattering or fluorescence/absorption in UV-visible regions of light spectrum.
Fun option is to develop chemical-reaction based assay. Say, engineer reaction that will modify histamine using radioactive-labeled compound and then measure how fast/slow amount of the compound decreases


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Are SNPs always in linkage disequilibrium with other SNPs
Is it possible to have a SNP that is not found is be non-randomly associating with any other SNP?

Linkage disequilibrim is a result of two SNPs both appearing after a cross (e.g. in offspring).  As such even at great distances two SNPs could both appear in offspring 50% of the time.  Linkage refers to a non-random odds that two SNPs (or any other marker) will both appear together in offspring. (Equilibrium being essentially random linkage).
By this definition, SNPs on different chromosomes should have no linkage.  Typically linkage reflects that there is a chance of a crossover between the two SNPs that would cause them to not co-migrate.  The closer together in general the linkage is very strong - a crossover appearing between two mutations that are just a few bases apart is nearly impossible.

There can be a number of reasons for Linkage Disequilibriunm (LD). Here is a non-exhaustive (non-referenced also) list.

Random LD happens
Epistasis
A recent selective sweep
Hybridization
Population structure
Genetic drift can also create negative LD (see Barton and Otto, 2005)

Of course, in all cases, reduced recombination rate will help to create an LD and to retain it for a longer period of time.


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Turning off the IP3 cascade
After PIP2 has been converted into IP3 and DAG by phospholipase C (PLC), some of the IP3 opens calcium channels in the endoplasmic reticulum and calcium ions can enter the cytoplasm. However, it is unclear to me how this IP3 cascade is terminated. Is IP3 somehow degraded, do high calium concentrations result in closure of the calcium channels or is there some other mechanism?

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

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

The IP3-DAG Pathway is triggered by an external stimulus that causes the conversion of PIP2 to IP3. When the stimulus is absent, the pathway does not function.
For example, TRH (Thyroptin Releasing Hormone) causes the IP3-DAG Pathway to occur in the cells in the Anterior Pituitary causing them to secrete TSH (Thyroid Stimulating Hormone) to the Thyroid Gland. When the Hypothalamus stops sending TRH, then the IP3-DAG Pathway in the TSH-secreting cells stops so TSH is not secreted.
Note: I am in high school right now so I may not have adequate experience in Cytology to answer this question. However, I tried my best!
Hope this helps :))

This does not answer the question asked. The question is wondering what happens to the IP3 after is is free to bind it's receptors.

Good  try and stay inquisitive.


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Do bees from different continents have different "taste"?
This question was already asked by me at Gardening Stack Exchange, but I was advised to ask it here instead. I see there is already a closely related question: Do animals have different taste preferences within the same species? . However, I would like some bee-specific clarification or study material, if possible.
I live in Europe, and planted several supposedly bee-attracting, but non-native (originate from Americas) perennials, most notably:

echinaceas
hellenuims
rudbeckias

For all species, I chose several cultivars, for the sake of experimenting.
Although all three species are listed as bee-attractive, bees at my place like only echinaceas and hellenuims. They totally ignore rudbeckias! Is there any plausible explanation for this?
Can it be that european bees are just not used to rudbekias, or simply don't like it, while american bees do?

Did you check the YT channel where he gives bees different types of water and nectar and checks which they go for?

No, but would definitely love to see that video, any link perhaps? Many thanks for idea/suggestion! @aliential

Probably bees communicate which flowers have the "most" amount of nectar, whereas the chemical makeup of it is a complex topic and probably a secondary choice option, they are picky about water though... https://www.youtube.com/watch?v=fVuxhp4TWNs&t=2s  bee dieting: https://now.tufts.edu/news-releases/bees-adjust-seasons-nutrients-flowers-and-dirty-water

I'm writing as a comment b/c I'm hypothesizing without examining the life cycles (are they even all flowering at same time?) or pollination syndromes of these specific plants. Bees, like all animals, need multiple nutrients (carbs, fats, proteins, etc), and their sources of each may differ. 1 flower may have  nectar richest in carbs and another maybe has a pollen richest in protein. Local surrounding plants might also provide better sources than your plants. The sources for each nutrient may also change throughout the year. In fact, the bees' actual needs may change throughout the year.

In other words, it's much more complex than simply planting bee-attracting plants.


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Is social anxiety a part of human gene pool and caused by natural selection?
I'm reading a book called 'Why Buddhism Is True' and I'm not sure I understand author's point regarding social anxiety and natural selection:

Our ancestral environment didn’t feature cocktail parties, slumber parties,  or  PowerPoint.  Our hunter-gatherer ancestors didn’t have to navigate roomfuls of people they’d never met or send their children off to sleep in homes they’d never seen, or give presentations to an audience consisting largely of people they didn’t know very well, if at all.
Just  to  be  clear  (and  at  the  risk  of  repeating  myself),  I’m  not  saying  that  social anxiety isn’t in any sense a product of natural selection. The ancestral environment—the  environment  of  our  evolution — featured  lots  of  social  interaction,  and  this interaction had great consequence for our genes. If you had low social status and few friends, that cut your chances of spreading your genes, so impressing people mattered, even if PowerPoint  wasn’t  the  thing  you  impressed  them  with.  Similarly,  if  your offspring  didn’t  thrive  socially,  that  boded  ill  for  their  reproductive  prospects,  and hence for your genes. So genes inclining us toward anxiety about our social prospectsand our progeny’s social prospects seem to have become part of the human gene pool.

So, from what I've understood, author claiming that the fact that we have social anxiety around people which we probably will never meet again is caused by the fact that in the past every social interaction mattered. Is it true from science perspective? I mean, the people who weren't social in the past would just die without passing their genes, how the social anxiety can become in the human gene pool in this case?
I always thought that social anxiety/confience it's just byproduct of all the events which happens with a child(if a child's social behaviour is positively reinforced then there would have less fear in regards to socialazing, public speaking, leadership etc).
PS: English is not my mother tongue, so I might formulate the question not clearly enough, so, it would be ideal if you can get additional context by clicking on the link and reading the chapter which the passage belongs to(6 pages). Just to be sure the answers aren't based on my interpretation of the author thoughts, but rather on the actual text of the book.

I think you are very wise to be skeptical of 'evolutionary' explanations of something like social anxiety, which could otherwise be explained by an environmental effect. In general, tread very careful around people making big claims based on evolutionary psychology - it makes hypotheses which are almost impossible to test. That statement in the book is pure speculation with absolutely no basis in evidence or theory as far as I know.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, we expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). ——— The wording of your question makes me think you don't have a good grasp of genetics and the (very complex) connection between genes and phenotypes — for this reason I encourage you to check out the links I'll post below. Thanks!

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

Short answer - Probably not.
When we talk about traits in evolution, we generally talk about things that are absolute (for example, you either have an attached earlobe or you don't). However, a psychological phenomenon as complex as social anxiety is definitely not controlled by a singular trait. Instead, a number of traits, if found, lead to the phenomenon (things such as physical appearance, susceptibility to sadness et cetera).
This is not to say that the phenomenon doesn't have its roots in genetics, some part of it might be controlled by genetics as well. But logically it's much more plausible that a psychological phenomenon such as social anxiety is dependant on environmental factors much more than genetic factors.
We hear countless stories of people who used to be socially anxious but bettered themselves by forcing themselves out of their comfort zones. This would not have been possible if the trait was genetically controlled.
One other thing to be wary of (as mentioned in a comment on your question) is the fact that many people use false claims of 'darwinism' in order to make their pseudoscience seem legitimate. There is no proof currently that proves it so, and probably never will be.

Welcome to Biology.SE! Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. ——— You make several incorrect statements for example your first sentence — many traits with a strong genetic component are quantitative (e.g. height) and thus are in now way "absolute". You also fall into the trap of assuming that traits result from either genetics or environment rather than the interaction of genes with environment. (cont)

Your answer is much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. Looking up references supporting your statements will also allow you to find and correct the errors in your post. Thanks!


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Human Stem Cells and Disease
Can human stem cells be stored for use by future family members as a way to combat generational diseases like diabetes

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Stem cells can be stored but that is an expensive alternative to generating them freshly. It has been shown that you can make stem cells from skin cells.
Theoretically, it would be much less expensive to store a piece of epidermis from a recently deceased relative than to make fresh stem cells and store those.
However, the research for generating stem cells from deeply frozen tissues is not there yet. Furthermore, the concept of using stem cells to 'combat disease' is not the right paradigm. It might even be said that some diseases (cancer) are the result of dedifferentiation gone awry.
Where stem cell transplants are used is in the replacement of bone marrow after total body radiation/chemotherapy to destroy marrow (in those cases where the disease has arisen in the marrow). In these cases we rely on the poorly defined process that allows cells to target their microenvironment.
For example, it would not work if marrow replacement cells decided to grow wherever they landed (lungs, liver,etc).
So stem cell storage is an option whose time has passed ,as our tech now allows us to make them.