text:
Fraction of channels open at equilibrium
I found the formula for the fraction of channels open at equilibrium for a three-state mechanism (Colquhoun's paper in the microelectrode book http://www.utdallas.edu/~tres/microelectrode/me.html)

k1 and beta are forward rate constants. k-1 and alpha are backward rate constants.
p1(equilibrium) = (Xa/Ka)(beta/alpha) / (1+ ((Xa/Ka)(1+beta/alpha)))
Can someone show me how to arrive at this by derivation. I tried and I got it wrong (obviously!!!).
Xa is the concentration of the agonist and Ka is the equilibrium constant k1/k-1

The mechanism given by the OP is renowned in the world of pharmacology and drug-receptor interactions, and is due to Castillo and Katz (1957). A very readable review of the history and importance of this mechanism may be found in Colquhoun (2006), published in Trends in Pharmacological Sciences. (For more great papers from the Colquhoun lab, see here)
If A is the agonist, R the vacant receptor, AR an occupied but closed form of the receptor, and AR* the occupied but open form of the receptor, the situation where an agonist must bind before the channel can open may be represented as a three state receptor model (unoccupied, occupied-closed and occupied-open) as follows:
$$\ce{A + R <=>[$k$_1][$k$_{-1}] AR <=>[\beta][\alpha] AR{*} \tag{1}}$$
We need to be more specific here, and define exactly what is meant.  Let $A$ be the concentration of free agonist (ie agonist not bound to receptor), let $AR$ be the concentration of occupied closed receptor, and let  ${AR^*}$ be the concentration of open occupied receptor.  In addition, let $k_1$ be the second-order rate constant for the association of agonist with unoccupied receptor, and let $k_{-1}$ be the first-order rate constant for the dissociation of agonist from the occupied, closed receptor. Finally, let $\beta$ and $\alpha$ be first-order rate constants for the inter-conversion of the occupied receptor between closed and open states, respectively. Rate constants may be thought of simply as constants of proportionality arising from the law of mass action (see below).
The OP asks for a derivation of the following equation,
$$p_1^{(equil)} = \frac{({\chi}_a/{K_a})(\beta/\alpha)}{1 + ({\chi}_a/{K_a})(1+ \beta/\alpha)}\tag{2}$$
where $p_1^{equil}$ is the fraction of channels open at equilibrium, ${\chi}_a$ is the total agonist concentration, ${K_a}$ is the dissociation constant (not the association constant) for the binding of agonist to the closed receptor.
The situation is very nicely illustrated in the following diagram, taken from Colquhoun & Hawkes (1995)

Derivation
Although Eqn(2) looks daunting at first sight, the derivation is surprising simple.
Let $R_t$ be the total receptor concentration. An expression for $p_1^{equil}$ (the fraction of receptor channels open at equilibrium) may now be written as follows:
$$p_1^{(equil)} = \frac{AR^*}{R_t}\tag{3}$$
As
$$R_t = R + AR + AR^*$$
Eqn (3) may be rewritten as follows:
$$p_1^{equil} = \frac{AR^*}{R + AR + AR^*}\tag{4}$$
The problem with Eqn (3) & Eqn (4), of course, is that they are pretty close to useless. The total concentration of receptor is unlikely to be known, and obtaining reliable estimates for $AR$, $R$ and $AR^*$ present almost insurmountable experimental difficulties.
By the law of mass action, which holds that states that the rate of any reaction is proportional to the product of the reactant concentrations (and where rate constants may be considered constants of proportionality), the following may be written assuming the system described by Eqn. (1) is at  equilibrium.
$$ {k_1}. A. R = k_{-1}. AR \tag{5}$$
$$ {\beta}. AR = {\alpha}AR^* \tag{6}$$
Let  ${K_a}$ be the dissociation constant for the binding of agonist to the closed receptor. From Eqn (5), the following may be written.
$$ \frac{A. R}{AR} = \frac{k_{-1}}{k_1} = {K_a} \tag{7}$$
Therefore:
$$ R  = \frac{{K_a} AR}{A} \tag{8}$$
An equation for the total concentration of agonist, ${\chi}_a$, may be written as follows:
$$ {\chi}_a  = A + AR + AR^* \tag{9}$$
The problem with using Eqn (9) to obtain an expression for $A$ (the concentration of free agonist) is that it makes the resulting equations very difficult to solve. As regards the algebra, the situation is make a lot simpler by assuming that the total agonist concentration is equal to the free
agonist concentration, ie by assuming that Eqn (9) may be written as follows:
$$ {\chi}_a  \approx A  \tag{10}$$
When the concentration of agonist is very much greater than that of the receptor, this approximation is justified.
Eqn (8) may be re-written as follows:
$$ R  = \frac{{K_a} AR}{{\chi}_a} \tag{11}$$
From Eqn (6), an expression for $AR^*$ may be obtained.
$$ AR^* = \frac{{\beta}. AR}{{\alpha}}  \tag{12}$$
By substitution for $R$ (using Eqn 11) and  $AR^*$ (using Eqn 12) in Eqn (6), followed by cancellation of the common term ($AR$), the following expression may be obtained:
$$p_1^{(equil)} = \frac{\beta/\alpha}{1 + {\beta/\alpha} + K_a/{\chi_a}}\tag{13}$$
Multiplying Eqn (13) 'above-and-below' by ${\chi_a}/K_a$ gives Eqn (2), the equation requested by the OP.
Comment
Note that when $K_a$  = $\chi_a$ and $\beta/\alpha$ >> 1, almost all of the receptors are open as $p_1^{(equil)}$ is close to 1.  When $K_a$  = $\chi_a$ and $\beta/\alpha$ << 1, almost all of the receptors are closed, as $p_1^{(equil)}$ is very much less than 1.
Note also that $K_a$ is a dissociation constant and is the ratio of a first-order rate constant and a second-order rate constant, and will have dimensions of concentration.
Addendum
It may be of interest that Colquhoun's great book, Lectures on Biostatistics, is (legally) available free of charge (as a pdf) from here
DC's Improbable Science
A great site

Thank you very much. I greatly appreciate the effort you have taken to show me the derivation.


text:
What would cause a single white eyelash?
I couldn't find a paper who could give me the explanation. Unfortunately, according to my search, it seems there are not many reported case, particularly for the younger population (<30). Would stress cause this?

Hair ( and eyelashes ?) comes in a spectrum of colors  ( at least for Caucasians ). In our lab we were testing a new microtome ( really good knife) ; A pinch of hair ( about 30) was pulled out of my head and sliced . The magnified image of the  dozens of round cross sections showed white, black, red , and 10+ shades of "brown" from light yellow to dark brown. Back when I had hair , the overall appearance  was light brown.

What Causes Hair to Have Colour and How is Colour Lost?

The colour of hair is due to the presence of melanin, which may be found as eumelanin or pheomelanin. Melanin is produced by melanocytes and is transported to keratinocytes. The hair then grows out from a root at the bottom of the hair follicle. A hair without melanin is a grey hair. The exact specifics of how hairs go grey is quite complex and poorly understood.
The growth and pigmentation of hair grows are both regulated by many factors, including genes such as MC1R and DLX3. This provides some explanation why people of particular ethnicities or families can go grey at different times - their genetic makeup changes how quickly they go grey.
Another factor affecting hair pigmentation is reactive oxygen species (ROS). The generation of ROS (oxidative stress) has been shown to have a role in the greying of hair.. Moreover, ROS are generated by smoking, which could lead to premature greying.
Other factors that have been found to be associated with premature hair greying include UV light, vitamin B12, iron, copper, ferritin, calcium and vitamin D3 (source).

What Would Make an Individual Eyelash go Grey?

As far as I know, the regulation of eyelash growth and pigmentation is very similar to that of hair on the scalp.
Given that the regulation of hair pigmentation is controlled by genetic factors, it could be that there is a change in the function of the genes at that particular hair follicle. This could possibly involve mutations which change signaling pathways, melanin generation, etc. such that melanin is no longer transported into the hair.
There could also be an extrinsic (outside of the body) factor which has locally stopped melanin production. Perhaps at some point, there was an elevated level of ROS or UV light at that particular hair follicle. This could have introduced mutations in the genes, or could have changed how the hair was pigmented.
Alternatively, there could be death of melanocytes in that specific area, which could stop the generation of melanin. There could also be a local change in the levels of the factors associated with greying (e.g. a local vitamin B12 deficiency).

Does Stress Cause Premature Greying?

Surprisingly, despite common knowledge telling us that hair makes us go grey, there is conflicting evidence about this. Stress has been shown to make us go bald earlier but whether it also makes us go grey is not conclusively known. But given that stress has a clear negative impact on health, it's probably best not to be too stressed regardless.

Regarding the reasons for this pigmentation change; would it be plausible to think that the eyelash can regain its original color following the improvements on the mentioned factors?

@matlabcrz I'm not certain but I think that's unlikely. If the melanocytes are dead, it seems unlikely that they'd come back to life. I'm not sure what would happen if the genes are altered. But hey, it's just an eyelash - it's going to fall out anyway at some point and it's not like anyone would notice that it's white! Plus, I know plenty of people with white patches of hair, and it's really not noticeable :)

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text:
What is this organism?

Link to GIF on imgur
What is this flat organism? It is around 1 cm long. I find them in places which aren't cleaned often. Location is India. Are they harmful or poisonous?
Edit: I've found that this is a duplicate question of What insect is this? (India).

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text:
How much arteries expand during systole?
Arteries expand during systole. By what percentage, on an average, does the arteries' diameter change during systole  with respect to diastole? Answer may depend upon type of artery i.e. elastic artery,  muscular artery, arterioles etc, you may specify the type.
This
https://www.google.co.in/url?sa=t&source=web&rct=j&url=https://www.nature.com/articles/eye199419.pdf%3Forigin%3Dppub&ved=2ahUKEwjuy4_Z2rvaAhWMYo8KHXuVAfcQFjAFegQIARAB&usg=AOvVaw3L27QesaUFNIqGfkINgy-7
paper shows 3-4% change in diameter of retinal arteries, but size of the arteries is roughly 100 microns. I am more interested in arteries with diameter more than 1 mm.

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text:
Sleep deprivation relation to growth rate and mental health in adolescence
Do sleep deprivation and its timing affect growth rate and mental health in adolescents? If so how much sleep is enough for teenagers?

Welcome to SE Biology. I am afraid that personal medical questions and health advice are off-topic here, and your question would seem to be asking for health advice. Please see the Help Centre.

@David i still think if Daulet reformulate this question as question with general meaning, I ll be able to answer this question.

@L.Diago — Then you need to explain to him how you think his question needs reformulating. My own opinion stands. If there is any SE site this is relevant to it would be Medical Sciences, but, like this site, that is supposed to be for professionals and serious students.

@L.Diago — I noticed that the poster used the "health" tag. The summary of that is worth reading: "Health and medicine questions are off-topic unless dealing with the biology underlying health and medicine. Please carefully explore the tour, help centre, and meta before posting health and medicine questions. Health is a physiological state of well-being referring to the (ab)normality of the cellular or organismal physiology."

@David but it can be take from circadian physiology point of view. Sleep deprivation And mental health Is pretty common topic in chronobiology.

@L.Diago — Well make and state your assumption of what a good question would be and give a good technical answer. My vote is only one of five needed to close a question.

@L.Diago Thank you very much for editing my question! : -)

@Daulet Aybaz i ll try produce relevant answer as soon as possible.

@L.Diago I would appreciate it!

@DauletAybaz i am sorry that it is taking so long, but i was really surprice about lack of articles on growth hormone regulation associated with sleep. Just saying that i wont ditch you.

@L.Diago Thank you for your work! I really appreciate it and waiting for your answer and info)

A couple of papers (from the same group, it seems) defines sleep deprivation in adolescents as less than 6hr of sleep within a month. They found that sleep deprivation increases health risks, importantly depression (which in turns increases sleep deprivation).

I think it needs to be pointed out, that defining sleep deprivation as less than 6hr and finding some detrimental effects says absolutely nothing about whether more than 6hr is enough.


text:
eosinophil question
Which of the following statement(s) is/are incorrect?
A. All cells of the immune system originate in the Bone Marrow
B. Lymphoid progenitor cells originate from a pluripotent stem cell
C. B cells develop in the thymus
D. Eosinophils are highly phagocytic
E. Both (b) and (d)
F. Both (c) and (d)
I suspect the answer is E, but I'm not entirely sure how phagocytic eosinophils are (I think it's pretty low b/c they mainly degranulate)
Reasoning:
A-correct because all immune cells originate from hematopoietic stem cells (HSC) from the bone marrow (BM).
B-wrong bc the HSC only gives rise to blood cells and is not pluripotent
C-Correct, B cells are differentiated in the BM, but mature in the thymus.
D-Wrong??, My lecture notes say that eosinophils are granulocytes (their main function), but google says they also phagocytose, so my conclusion is that they are NOT highly phagocytic.
->>> answer = E?

Did you google any of this? If so, what did you find out? (Showing your research - not just what you suspect - is pretty much required in questions here, or it will be closed as a homework question.)


text:
Is starch a better coagulant than cellulose?
In an experiment, I used plantain peels (with a very high starch content and very little cellulose) and grapefruit peels (with a very high cellulose content and no starch) as coagulants (ensuring that I used equal masses of each peel) to improve the turbidity of water contaminated with wood chips and kaolin. Although the grapefruit was able to remove turbidity, I found that the plantain worked better. By the way, the same amount of cellulose was present (50%) in the grapefruit peels as starch present (50%) in the plantain peels. However, I can't work out why a coagulant concentrated with starch is more effective at lowering the turbidity of water compared to a coagulant concentrated with cellulose? Essentially, I don't know why starch helps more than cellulose with coagulation. Help would be much appreciated :)
If you use this link, you will find the method I used under "Preparation of Bio-flocculant" to turn the peels into coagulants: akademiabaru.com/doc/progeeV1_P47_56.pdf. To summarize, I dried them in an oven and turned them into very fine powder.
Search this up and you'll find previous experiments using polysaccharides (i.e. starch and cellulose) for coagulation: Chapter 2 Mechanistic Insight into the Coagulation Efficiency of Polysaccharide-based Coagulants

Did you use equal mass of each peel? If you didn't account for differences in content it could be that the plantain peels contained more starch per kg than the grapfruit peels contained cellulose per kg. Were the peels just tossed in or macerated, how were they pre-treated? Starch from the plantain peels may dissociate into the water faster than the grapefruit peels, for example.

Yes, I used equal mass of each peel. If you use this link, you will find the method I used under "Preparation of Bio-flocculant": http://www.akademiabaru.com/doc/progeeV1_P47_56.pdf. To summarize, I dried them in an oven and turned them into very fine powder. The same amount of cellulose was present (50%) in the grapefruit peels as starch present (50%) in the plantain peels.

@Julie please [edit] the question to add all necessary details instead of answering in comment. Also, please add a link to the reference that you cite.

Sorry long work day, what's your sample size? Does n=1?

What do you mean by sample size? I repeated the experiment three times, adding the same mass (4g) of each peel into the solution.

Please do not expect people to do the web search to find out the details. All the necessary details should be contained in your question.


text:
The effect of Atrazine on the LDR in Photosynthesis
The herbicide Atrazine causes inhibition within the Qb site in the D1 protein of photosystem 2.   Given this information, would Atrazine’s inhibitory effect halt the production of oxygen or ATP first?

Given that water is oxidized indirectly by P680+ and the build up of intermediates caused by inhibition in Qb  would not allow P680 to deposit its extra electron into the beginning of the electron transport chain, water would not be oxidized/split into 2H+ and (1/2)O2 because P680 would not become P680+.   So this inhibition would halt the production of oxygen, correct?
Given that, I would say that the production of O2 would be more immediately halted than that of ATP, especially since ATP synthase would continue to function until the electrochemical gradient between the stroma and thylakoid space was spent, and would not be immediately affected by inhibition in Qa (although the electron transport chain which maintains the electrochemical gradient would be compromised and thus indirectly ATP synthase would be affected).
Is my reasoning correct?


text:
How are single cells sorted in an scRNA-Seq protocol by FACS?
I am computational guy trying to understand how FACS sorting works in an scRNA-Seq protocol. About sorting single cells in each well of a 384-well plate, I have a question that would be grateful if you could answer it.
The protocol reads that cells are sorted in the wells based on their marker levels. For example it says:

NK single cells were collected from the CD19-/TCR-β- events by gating
  for NK-1.1+ events in NK-1.1 vs. Gr1.

The part that I don't understand is that how it is possible to know positive/negative events or even to gate on events beforehand? I know that FACS first examines markers and then sorts them into positive, negative or waste collections. Here is my question:

But how do we know what an expression level is acceptable for calling
  a cell positive, and also in more complicated case, how do we to gate
  on a subpopulation of cells (like top right quadrant) when no events
  have yet crossed the laser beam because we don't know the baseline of
  CD markers' expression levels yet?

For instance, It could be possible that in my panel setup a CD marker can never reach a value more than X, but in your setup it can never reach a value more than X/2.
N.B. As protocol says, subsampling of the main sample for FACS is not possible to infer these values beforehand because it is very likely that the populations of different cell types is not conserved in the subsample.

I will append the previous sentence in your protocol, and put what might help you in bold:

To  obtain  B  cells,  NK  cells  and  monocytes,  a  splenocyte  suspension  was  stained  with PE-Cy7-conjugated  CD19,  eFluor  450-conjugated  NK-1.1,  PerCP  Cy5.5  Gr1,  FITC TCR-β,  APC  CD11b  and  PE  B220  (CD45R).  B220+ and  B220neg (germinal  center)  B cells  were  collected  by  gating  for  CD19+(TCR-βneg)  cells  and  then  by  B220  against  theCD19  marker.  NK  single  cells  were  collected  from  the  CD19neg/TCR-βneg events  by gating  for  NK-1.1  positive  events  in  NK-1.1  vs.  Gr1.

The cell types in question have unique properties that can be stained for using (immuno)histochemistry, i.e. chemicals and/or antibodies. The antibodies themselves tend to be conjugated, i.e. they are covalently bound to fluorophores typically which are fluorescent. That means a cell type can be labeled by fluorescence, and the FACS machine can sort fluorescent cells from non-fluorescent cells.
They stained the different cell types with different markers. The markers are sufficiently different from each other to be able to use them together in some cases. For instance, whatever FITC is could be used simultaneously with PE-Cy7-conjugated antibody.

First, they collect two subsets of B cells (the B220 positive and negative cells) by using the CD19 marker (PE-Cy7-conjugated antibody that binds CD19).
Then, from one of the subsets, the B220 positive one, they sort another subset which is positive for eFluor 450 (which is conjugated with an NK-1.1 antibody). This collected subset fulfills their criteria for being NK cells.
This subset is used for single cell capture on a plate (e.g. for SMART-seq2) or using microfluidics (e.g. for 10X Chromium).

For a FACS machine, you can select the threshold level of e.g. florescence that will be used as a cutoff between positive and negative events (cells). This is arbitrary and is usually subject to trials.

Thanks for your answer, but someone told me they do index sorting today for scRNA-se but I don't understand it wither! :-)

I think index sorting is when you sort the cells into individual wells, and each well or cell is assigned its fluorescence value (each well is indexed). Then using this data in retrospect, you can choose which cells/wells you want to combine or eliminate. I'm not entirely sure but I think that's the gist of it.

we don't know the baseline of CD markers' expression levels yet?

There are standard settings that can be used between runs that will give consistent results from one sample to the next. There are also controls (fluorescent beads) that can be run beforehand to set the machine to ensure that those standard settings will work, and that allow you to make the relatively minor adjustments to bring them into a consistent range.
But you also have another misapprehension:

subsampling of the main sample for FACS is not possible to infer these values beforehand because it is very likely that the populations of different cell types is not conserved in the subsample.

Just because the positive cells are not in the subsample doesn't mean you can't set normal values.
The key is that a positive cell isn't a subtle thing. In a typical flow cytometry stain, your positively stained cells will be much brighter than your negatives; at worst tens of times, often thousands of times brighter. Setting a gate fairly close to the upper end of your negatives (in your subsample) will in practical terms guarantee that your positives will be outside the gate.
I grabbed a random example from a Google search; this is a pretty typical looking gating:

Notice that in each gate, the positive population is (eyeballing) a thousand times, to several thousand times, brighter than the negative (the X axis is a log scale). When you have that much room to work with, delicate subtle effects in baselines settings can be safely ignored.

Thanks for your answer, but someone told me they do index sorting today for scRNA-se but I don't understand it wither! :-)

Index sorting, very simplistically, is just a retrospective analysis of the cells that are sorted. You collect single cells without a specific sort (or more typically, after they are sorted for many but not all parameters); you perform some other kind of analysis on the cells (like sequencing); and then you go back and link the full analysis of the cell, to the further data you collected. It means you can assess parameters that you didn't explicitly sort for.


text:
Freestyle Libre's Glucose's Specificity and Accuracy?
I am studying the Continuous Glucose Monitoring devices i.e. glucose sensors with continuous monitoring.
Here one good presentation about the topic.
They are considering interstitial fluid in their analysis, which I think is risky, probably more risky than Theranos product, discussed here.
Characteristics

measure oxygen in interstitial space and estimate blood glucose
sensor current average efficacy 10-14% which is good but not enough

Sources

Sandeep Kumar Vashist, 2013. Continuous Glucose Monitoring Systems: A Review.

How can FreeStyle Libre glucose test's be specific and accurate compared to conventional blood-glucose devices?

Interstitial glucose sensors can be reasonably accurate, but there are two main concerns: the sensor response time, and calibration.
Glucose diffuses from blood into the interstitial fluid, and it can take some time during periods of glucose change (e.g. after a meal) for an equilibrium to be reached. Hence, the sensor measurement will lag behind the true blood glucose level. The blood glucose is what people are generally interested in, so measurements of interstitial fluid are used to estimate the blood glucose level, and so are only valid during periods of stability. With careful management of sugar intake this can be an acceptable compromise however.
Most CGM sensors require calibration against a reference instrument such as a test strip-based device using a finger-prick blood sample. As long as this is done during a period when the interstitial glucose level is stable, the sensor can hold calibration for several hours and indicate the trend in the blood glucose concentration.
The Theranos product is something completely different, and isn't suitable for day-to-day monitoring of blood glucose levels. The samples are sent away to their lab, so there is a delay in receiving results. They will measure your blood glucose level but this would generally be a fasting measurement to provide a background level. Nevertheless, this (should be) a more accurate test, as it is laboratory based and takes a physical blood sample.
CGM sensors have been shown to be accurate to within clinically useful ranges, when used with the above considerations in mind. Specificity (and sensitivity) are only really considerations when test results are compared against cut-offs to determine a positive/negative result. This paper is a good summary:
http://ceaccp.oxfordjournals.org/content/8/6/221.full


text:
How much Cardiomyocyte Move in Relation to its Neurons?
I am trying to estimate how much cardiomyocyte and its things (mitochondria) move in relation to neurons

Movement of neurons (1)
Movement of cardiomyocytes
Movement of cardiomyocytes' mitochondrias (2)
...
Movement of stem cells - I think we can ignore this one

Motivation: some imaging projects have focused on the neurons etc ECG/... because they move relatively little in comparison to cardiomyocytes and their organelles; my interest is in the electromuscular view and I would like to understand how the movement of cardiomyocytes and their mitochondrias could be adjusted/calibrated in the time-frequency (t-f) data (spectrogram/...) of cardiomyocytes
Pseudocode
Simplistic view about including the effect of cytoarchitecture of organelles on the dynamics/movements based on statistics and probabilistic approaches
function getMitochondriaDynamics2D(signal2D, edges, Cytoarchitecture):
signal2D=$1;
edgesN=size($2,2);
organelles=[neurons, cardiomyocyte_minus_mitochondia, mitochondria, ...]; % given
organelles.cytoarchitecture = $3; % probabilistic values in Statistics
organelles.dynamics = zeros(1,edgesN-1); % preallocation

% Limit dynamics by cytoarchitectural restrictions
for organelle in organelles
    % include here systemic effects on organelles but Ignored here
    % etc Age, Smoking, ...

    % Let's loop local changes
    for edge in organelles.dynamics
        organelle.dynamics(edge) = organelle.dynamics(edge) .* ...
            organelle.cytoarchitecture(edge);
    end
end

return signal2D .*organelle(mitochondria).dynamics;

end

%% TODO here
function analysisMitochondriaDynamics2D(dynamics2D)
    ...
end

To find those probabilistic values

Embryology but I am weak here
databases and/or publications - which?

Biochemistry
I do not understand how much this should be considered here, but it could help to get any model

Atrial cardiomyocyte calcium signalling
mobility of the delayed-rectifer K+ channel Kv2.1 (3)

Useful keywoards

cardiomyocyte adult mobility

Hypothesis and Math/Physics/Bio
Hypothetical View of t-f data (2D) in cardiomyocytes: regular points separated by steady-gel-like areas - - seems to artifact of the movement
Physics about characterizing such areas:

... [ which mathematical methods ] ...

Sources
There are much studies in Embryology about cardiomyocytes and their movement, but I cannot understand their relation in the topic

Piquereau, Mitochondrial dynamics in the adult cardiomyocytes: which roles for a highly specialized cell?, 2013
How to measure Na/K channel activation at the membrane level?
Localization and mobility of the delayed-rectifer K+ channel Kv2.1 in adult cardiomyocytes.
Mitochondrial dynamics in the adult cardiomyocytes: which roles for a highly specialized cell?
PubMed with cardiomyocyte+"patch clamp", about measuring plated cells which are from hearts freshly minced in collagenase / EDTA. See PMIDs 27364017, 27076034, 26142302, 26241168, 26378152, ... [NickSandor]

Useful keywords

adult cardiomyocyte
possibly: Atrial cardiomyocyte calcium signalling
Mitochondrial dynamics
cytoarchitecture restrictions dynamics


text:
Fast standing and the heart's insufficient accommodation of the increased venous return
Assume you are 45 minutes on the supine position. Furthermore: you stand all of a sudden and fast and without sympaticus activity.
The venous return (smooth musculature of vessels) accommodates faster to the change (decrease of venous return) so returns blood to the heart before the sympaticus has accommodated for increased cardiac output.
This creates a significant increase in the blood volume entering the heart.
In pathological situation where systemic vasoconstriction not occurring normally, the heart is not capable of handling the overdistension; resulting in a pain during the second cardiac cycle.
I am interested in knowing which phase the heart is most vulnerable:

filling,
isovolumetric contraction
ejection
isovelumetric relaxation

or more explicitly (from my answer here)

Atrial systole
Isovolumetric ventricular contraction
Rapid ventricular ejection
Reduced ventricular ejection
Isovolumetric ventricular relaxation
Rapid ventricular filling

I think filling can happen normally, but not with the sudden isovolumetric contraction (most sympathetic innervations here, so therefore I think this is the weak link).
When there is too much blood in the ventricles, some of the blood is reflected back from the ventricles into the atria causing a painful sensation and possibly tachycardia (as well as an possible increased risk of atrial fibrillation if such events happen regularly).
Is the isovolumetric contraction (systole of ventricles) of the cardiac cycle the possible weak link in accommodating a sudden increased venous return?

When you stand up suddenly from a supine position, venous return to the heart will decrease, not increase. Moreover, heart chambers overdistension does not cause pain. What will happen when standing up is that systemic vasoconstriction will occur to maintain blood pressure until the venous return can be adjusted.

@Raoul I agree with every sentence of your comment. I used little bit overloading in my language. I made it now more explicit. However, my case is a pathological situation where the musculature is not able to accommodate and thus causing a pain.

If you get retrosternal pain, it means myocardial ischemia is occurring, for whatever reason. I do not think ventricle overloading or blood regurgitation per se can cause pain.

@Raoul You are right again. I added my explanation and answer about the case here. I think prolonged undiagnosed celiac disease can cause symptoms that remind those of retrosternal pain.

Raoul's gives sensible comments:

ventricle overloading not sensible
retrosternal pain $\to$ myocardial ischemia
other cause reminding retrosternal pain such as celiac disease:

Posterior 1/3 of the septum is supplied by the following artery where any ischemia can weaken the isovolumetric contraction (TODO this has to be discussed much more carefully):

ischemia coronariaea posterioris created by problem in ramus interventricularis posterior arteriae coronariae dextrae


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Explaining "paraphyly" for the layperson?
I was a molecular biology major a while ago, but I never think I really understood cladistics TBH. Now reading about paraphyly, it shows this:

In this phylogenetic tree [second image], the green group is paraphyletic; it is composed of a common ancestor (the lowest green vertical stem) and some of its descendants, but it excludes the blue group (a monophyletic group) which diverged from the green group.

Looking at the "simiiformes", I can understand why you would call that "monophyly", because everything is connected to a common ancestor. But why not just make the blue area a full blue triangle to make the prosimii and simiiformes one triangle/group? In the end, we all share the same ancestor, so I don't see why they are disconnected.
TBH I'm not sure how to read this at all, and am not following the Wiki description. Can you explain how the 3 terms work for a child or layperson with a better concrete example?
We are all composed of atoms, so we are all made of matter. Matter is made of particles, so we are all made of particles. But light is a particle and we are not made of light, even though in some way "we share the same common ancestor" of the quantum field. But light is still called a particle, so the triangle is the group of all particles. I'm not sure I'm getting on the right track.

A paraphyletic group is a monophyletic group from which one or more subsidiary clades (monophyletic groups) are excluded to form a separate group.

Why would they do that?

I don't think any child or layman will ask for an explanation of "paraphyly" ;)

"We call all of these 'trees', but actually they are a wide range of unrelated plants."

@KevinKostlan - your layman's explanation is more charitable than mine, which is "Taxonomy is a giant sham, genus/species etc is a description that, as we dive into the genetics, is harder and harder to force into reality. So we keep screwing with the data to try and make it fit, because "new species" is a concept the public think is cool, whereas "genetically distinct group" is not. Yes, it's messy. Blame the swedish pedant working before genes were discovered for it."

Or, less ranty - "In this case, the genetic data tells us there three distinct groups in Prosimii. However, because they all have similar features, we'd like to lump them together for identification and historic reasons. It's clear they don't particularly fit, and in the case of  Lorises and Tarsiers, their grouping is in no way more closely related than Lorises and Lemurs, but this is how we can get things to fit with the existing taxonomy classification

@Lupe: "Taxonomy is a giant sham". Does it matter whether we consider a Texas cougar the same species as a Florida panther (or that there is admixture)? I think it's more important for the public to realize that "invertebrates", "trees", etc are meaningless groupings, while "bird", "bony fish" (with very few exceptions), "insects", "mollusks", "flowering plants", etc are meaningful. Still other words are half-truths: "reptile" excludes birds, but "reptiles+birds" is a clade.

@KevinKostlan was a reason "taxonomy is a giant sham" didn't make it into my answer! Was being a bit factious. But, I think it's reasonable to argue that there are, at this point, such significant issues at every level of the taxonomic model that if it was less well established, we'd chuck it in favour of something better. I think it's important to acknowledge when we talk about it that there are great big holes in bits of it, too, which helps make more sense of its contradictions

These are terms to describe names we give things that don't really follow phylogeny accurately. Fish, for example - a monophyletic group involving fish would include humans, too, yet there are many cases where it's useful to talk about fish without meaning every land vertebrate, too.
From the page you link to:

The term was coined by Willi Hennig to apply to well-known taxa like Reptilia (reptiles) which, as commonly named and traditionally defined, is paraphyletic with respect to mammals and birds. Reptilia contains the last common ancestor of reptiles and all descendants of that ancestor, including all extant reptiles as well as the extinct synapsids, except for mammals and birds. Other commonly recognized paraphyletic groups include fish, monkeys, and lizards.

If you want to use any of these labels: fish, monkeys, lizards, reptiles, it's useful to have a term to describe how those labels relate to phylogeny, hence the term paraphyletic.

The quote seems a bit circular: "paraphyletic was coined to describe taxa which are paraphyletic"?

@terdon I'd paraphrase instead as "paraphyletic was coined to describe taxonomical words already in use". For reptiles, the quote also points out which specific taxa make "reptile" paraphyletic: mammals and birds, which is extra information and not circular.

One very simple example that most people are familiar with is the vernacular use of "animal". Most people recognize that humans are animals and more closely related to other animals than plants. However, usually when people say "animal" in everyday speech, they mean what would technically be called "non-human animals". "Non-human animals" are a paraphyletic group, including the last common ancestor of animals and all their descendants, but excluding humans.
While fish and reptiles are good examples, due to strange tendencies of popular culture, I think that laypeople are more familiar with birds being descended from dinosaurs than mammals being descended from fish. So you could say:

Since all birds are descended from dinosaurs, you could rightfully call birds "dinosaurs", and sometimes scientists do. However, when a five-year-old says "dinosaur", they aren't typically thinking about birds but referring to a paraphyletic group: extinct scaly creatures, maybe with some feathers, but excluding modern birds. Scientists sometimes say "non-avian dinosaurs" to make this explicit.

I put some comments further up, but if I was teaching this, my first attempt would be to "acknowledge the absurdity" - basically, that these groups clearly don't, according to the genetics, fit together.
The next bit is to talk about physical similarities - what features do the creatures share that might make someone group them together?
Then I think we'd talk about how we have two different classifications we're trying to reconcile - traditional taxonomy, which is how the entire body of research we have before genetics is organised, and modern phylogenetics.
Taxonomy groups creatures by physical features, and is broadly qualitative. It is produced by the determination of taxonomists.
Phylogenetics groups by nearest common ancestor, and is based on hard genetic data. However, it tends to ignore large physical features.
Polyphyly is just an area where two groups identified by taxonomy as closely related, share less common ancestry than a group that was not included by taxonomy - it's a taxonomic screwup, but one we can't simply fix. In time, as taxonomy is revised to take into account genetics, it is likely to be resolved, but that takes an extremely long time.

To answer your specific questions

But why not just make the blue area a full blue triangle to make the
prosimii and simiiformes one triangle/group? In the end, we all share
the same ancestor, so I don't see why they are disconnected.

They are one group, called primates.
That is not an image of all the clades for those organisms, it is just an example of the types of groups. Clades can be nested. The link below may help you. Cladistics is a organization of ancestor not just arbitrary categories. A clade is literally often defined as Organism X plus Organism Y, their Most Recent Common Ancestor, and all of its descendants.
Also names for groups have history including decades of published papers refering to them. you can't just change what a name is referring too every time we learn something new. Prosimii may have been thought to be monophyletic at one time, relationships change as we learn more about them. Or it could have been named for the things in one group but not in another, because that was something useful to talk about, like lawless fish. groups have history, a paraphyletic group might all be extinct making relation ships difficult to establish or not important for the characteristic being discussed.

https://evolution.berkeley.edu/evolution-101/the-history-of-life-looking-at-the-patterns/understanding-phylogenies/
Using anything that does not reproduce as an analogy has a big problem, for instance changing what is or is not a planet does not make a prediction about what the origin of all those planets/not-planets are. Cladistics is a map of ancestry and evolutionary history. A paraphyletic group might still be useful if everything in the group is extinct or lives on a different continent, or share similar features. Consider the terms non-human primate, non-avian dinosaur, or non-tetrapod fish, those are groups that are paraphyletic,  but still useful groupings to make for discussion. They are abasically ALL X that do not have feature Z.

I would use reptiles as an explanation. Most people think they "know" reptiles (though they may mistakenly exclude turtles). So tell your layperson that birds are actually reptiles. If you exclude birds, it is just like having some cousins who look very different, so you decide they are not a part of your family! But that would obviously be false. In the same sense, the group 'reptile' is false, since it excludes birds. We call such false groups 'paraphyletic' because it sounds more academic than the phrase 'false group'.
It turns out there are many, many false groups as people were putting living things into categories for centuries before we had readily available DNA sequences.


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How to teach my self Biology and Chemistry?
Long story short I'm a American dreamer (a immigrant brought to the USA as a child but is illegal) and recently returned to my home country and not knowing the language here have had a hard time at school I am now 22 and think I can finally get somewhere I just need to teach my self Biology and Chemistry (Childhood dream was to be a biologist of some sorts) but I don't know where to start.
Can anyone recommend and books how how I should start my studying? I need to learn this stuff to be able to get into a university here. I wan't to start from the start and work my way up to University level.
Any sort of help would be greatly appreciated
Thank you in advance
Edit: TLDR: Basically I'm asking how I can home school my self to learn Biology and Chemistry to be able to get into a University and learn Biology and Chemistry on a University degree.

Possible duplicate of Books for beginners. There are also other posts that are more specific (such as Very introductory online source of information in evolutionary biology e.g.) that can be of interest to you.

I am sorry you've been evicted from the US to a country you know little about and don't speak the local language. As unfair as this situation sounds to me, I would like to reassure by saying that you will quickly learn this new language and will be able to attend classes like anyone else. Hopefully, this country has a decent education system and you will be able to pursue your education as you please.

For chemistry, please see on chemistry.SE

The stated clearly series is a good introduction to evolutionary concepts,  https://www.youtube.com/channel/UC_cznB5YZZmvAmeq7Y3EriQ. Personally I like Richard Dawkins books like the selfish gene and the extended phenotype, they are also fairly easy to come by.


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Do fallen leaves produce oxygen?
After a leaf has fallen from a tree, if it is still green and hasn't dried out, is it still converting CO2 into O2 if not put in water?
Can anyone find any data showing how long any different species of leaf will continue to produce oxygen after fallen?

Short answer
It all depends on the time window you are talking about. After having been detached from the mother plant, a leaf will typically keep on photosynthesizing for a few hours or so.
Background
Cutting of the stalk of the leaf results in impaired water flow and wilting. As soon as a leaf is detached from the plant, it will also be cut off from hormones, minerals and other nutrients. The result of this is that senescence (and death) sets in straight away. However, leaves will typically stay green and moist for hours or even days, dependent on the conditions it is stored. Hence, in practice, photosynthesis can be measures at least a few hours after a typical leaf is picked (source: Science and Plants for Schools).

Thanks so much. Any more-detailed information showing exactly how long they will continue to photosynthesize?

@Johan88 - depends on species, and conditions (heat, humidity and so forth)

that's exactly what I'm thinking, but I hope I can get some data from some studies, but have not been able to find any such studies.

It would be a nice experiment to use CO_2 with radioactive C14 isotope in an artificial atmosphere to measure it, or you can measure the increase of humidity (much easier, but less crazy scientisty and accurate). btw. the saddest biology question ever :( poor leaves...

Note that there are many plants where if you cut off some part of it and leave it lying on the ground, it will grow roots and become a new plant.

@atevm Hahaha. The saddest Biology question Kakaka. Well, the leaves fall around me all the time, and I like to pick them up and put them in a bowl in the hopes they can still create oxygen for a while and their life isn't over yet  :)

@Johan88, seriously, you are not kidding?  There is plenty of O2 and as long as things like CO2 concentrations stay stable or better RISE in ppm plants and the ocean will continually make O2.  There are far better ways to expend your energies!

Every single thing that was once alive, once dead, once cut off begins to decompose immediately.  Fully is the temperature is correct.  O2 is produced during the day as long as there is CO2, tiny tiny amounts of chemistry (NOT NUTRIENTS), water, drainage in the soil medium, ventilation...actively photosynthesizing chlorophyll produces oxygen, 'sinking' the CO2 within its biomass.  Just like the ocean.

https://www.youtube.com/watch?v=CrrSAc-vjG4 This would be fun for you to watch if you've not watched already.  When they say the words, 'food for plants' I want you to hear me scream!!  Otherwise, great documentary.

@stormy truth be told, I'm not allowed to bring plants where I work: boss would consider it inappropriate. Modern decor: the air REEKS of plastic and fumes and I absolutely hate it and feel nauseous. I pick up fallen leaves in the morning and stuff them where they have some light and won't be seen. Hope it improves oxygen. Certainly has a placebo effect if it doesn't. Need some damn green! :P I dump em when they're dried out since decomposition does the opposite I think: O2 to CO2

Ah, Johan, you are describing a true nightmare.  Decomposing leaves don't provide oxygen.  The smell of earth, of rot and decay, 'centers' you.  Something like that. Sigh and major sigh.  I would be working on a major change for you...I hate money. Anyway, You need to get your hands in the dirt after and before work.  You need to 'work out'...cardiovascular mostly.  Walking, running, bicycling.  That will help you keep your objectivity.  I get it, I do!  You are the only one who decides the directions of your life.  You be honest with you and take care of you firstus!

@stormy Thanks. When I said "Need some green" I meant need some green life, plants, even if it's just a few leaves I pluck each day, despite my modern square plastic concrete boss and her rules. Lol, she caught a sight of a small leaf pile the other day and was like, "What's that?" "It's my oxygen machine. Cannot?" "Really?" "Cannot?" "REALLY?" "The air quality is so bad. Cannot?" "Get rid of it on your lunch break." Currently I'm hiding an airplant somewhere. Lol. Good things my boss's boss likes me, otherwise my little quirks would not be tolerated.

Johann...it is nice your boss likes you, needs you.  You sound as if you need to be self employed.  Photosynthesis produces oxygen but there is plenty of it around, you don't need to make anymore.  Decomposition doesn't produce O2 it uses it during aerobic decomposition.  You are so dang cute.  Hiding an air plant.  Seriously, life is too wonderful to waste a single minute working FOR someone else in an environment that is driving you nuts.  Huggs.  You and your little quirks need to find a new home where appreciated!

https://www.researchgate.net/profile/Rien_Aerts/publication/216809762_Climate_Leaf_Litter_Chemistry_and_Leaf_Litter_Decomposition_in_Terrestrial_Ecosystems_A_Triangular_Relationship/links/54412b640cf2e6f0c0f60201.pdf

@stormy self employment is the plan. In HK, in the heart of the city, kilometers of concrete and asphalt all around me in every direction, air pollution is terrible. I want the plants for air cleaning (fumes and chemicals) more then oxygen. My boss doesn't like me. She fears me. Because her boss fears me. Because the former boss of the boss of my boss loves me. It's complicated. I'm aiming to launch my own business. I'm not against hierarchy at all, in principle. The problem is toxic personalities when you encounter them. And I want to employ people below me, and be a great boss. Thankyou hug!

You said the magic words, "they fear you"....this is a good thing as well as very bad.  If you are unable to get support, you've been boycotted.  Try to become less visible.  Less, grins, scary?  You will have to lead, and the more experience you've had with other humans the better a leader you will be.  Toxic personalities is not a helpful perspective.  As a leader you will be making these 'toxic' people into productive happy people, all part of a team.  Objectivity is a crucial skill. Sit down or lie down and imagine where you want to live and how you want to affect the world around you.


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Minimum number of cycles for effective qPCR quantification?
I have been having an apparent problem with gDNA contamination in my no-reverse transcriptase (NRT) controls by the appearance of fluorescence peaks in my qPCR data.
I have/am trying multiple DNase treatments (Turbo DNase, Life Technologies) and RNA-clean up (Qiagen, RNeasy). The limiting factor I am worried about is that I am going to destroy all my available mRNA with multiple treatments/clean-ups.
My question is - can I lower the number of cycles I use to measure fluorescence? Is there an aspect that will go awry (in terms of the experiment itself to data analysis) if, let's say, I lower the number of cycles to 25-30? All of my contaminations start to appear within the range of roughly 30 cycles and above (as determined by the Ct values).
Please let me know if you need any other information that could help for an answer!
Best

Are your targets getting into the exponential phase above background before your contaminants are?


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Might new bones evolve from soft tissue?
I wonder how bones evolve where there are none. (This is the question, read the sub-questions as examples :) )
Lets take an elephant as an example. If it was adaptive for the elephant, could bones somehow evolve in their soft-tissue trunks? If so, what tissue would they develop from?
Perhaps the sheet of cartilage in their ears are more likely to somehow calcify and become a new bone?
And would then several connected bones and joints evolve from the new bone tissue?
Is it very rare for new bones to evolve from scratch? Or, do today's bones entirely trace back to the set that evolved in early tetrapods?

I remember being curious about how bones were made and I eventually found out that bones develop from cartilage, so bones develop from cartilage. Is this what you were looking for?

New bones do form occasionally so it is not impossible, Ornithischian dinosaurs are defined by a evolution of a new bone (predentary). There are many pieces of cartilage in the body that become ossified in some animals and not others, the kneecap is a great example since a bony kneecap has evolved and been lost many times independently, it is just a matter of ossifying existing tissue. The trunk however is more difficult since it does not have any suitable cartilage.
Cartilage however is not necessary to form bone, but it is the most common way to get it. Endochondral ossification forms bone from cartilage and is responsible for the majority of the bones in the body. Intramembranous ossification forms bones in other connective tissue, the bones of the skull and dermal bones are examples of this process. Dermal bone has evolved separately many times but tends to form in the skin.
Given enough time  and the right selective pressures it is certainly possible for bones to evolve in the trunk but it is not going to happen quickly.


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Why do many cells together survive better than one cell alone?
I know that one cell with no ECM is subject to anoikis. That's why in general one cell alone not in its environment is dying.
But are there advantages for a cell to live close to other cells even of the same type (for many types it looks obvious) ? If yes what are they and could you give a reference if it is possible please ?
I don't mean only what evolutionary advantages do cells together have over one cell (which is more simple, and there is a wikipedia about it), but I'm more interested if one wants to culture cells that you find generally in tissues, why is it better to take many of them (because it is better, right ?) ?
To be clearer, my point is that I want to understand the mechanisms of what happens when cells (of the same type) are in community and to understand given those mechanisms the advantages a cell has when it is with other cells rather than alone.
Thanks !

Some cells need contact for survival. Is your question about why such a need even exists? I would guess that many cells have to form a uninterrupted layer for performing their function (for e.g. epithelial cells).

@WYSIWYG Could you give me a reference like a book or something plz ?

It's not really clear what you're asking.  There are certainly a great many single-celled microorganisms that survive perfectly well on their own.

@jamesqf well I'm talking about cells that one can find in tissues in general.

@J.A you haven't still clarified if you are looking for the "how" or the "why". BTW, have a look at this article for some info on "how". You can find more articles on Google Scholar.

Thx ! The question is more "how". Actually I understood that the "why" you were talking about was more an evolutionnary point of view. My point is that I want to understand the mechanisms of what happens and to understand given those mechanism the advantages a cell has when it is with other cells rather than alone.

@J.A okay.. Then I shall convert my comments to an answer soon. You also please [edit] your question to highlight that you are looking for the mechanism.

Cells can communicate with each other using chemical signals.
But do you also know about gap junctions? These are tunnels that connect cells in tissues.
Water, ions etc. can travel to and fro.
Or maybe a tight junction can connect cells together to form an an organ. No fluids pass through, which is good: The bladder is an example.


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What is this insect I found in northern Europe?
Found this one in my bed in Northern Europe.

Around 6 mm long (5 mm body + 1 mm nozzle). Seems to have 6 legs. The back looks a bit like black-brown camouflage, the legs are red-brown, the nozzle is black.
Could this be some kind of bed bug?

Possible duplicate of Small black slow-moving insect showing up in the home

The nose is a dead giveaway: it's a weevil. See this post for identificaron and info on bed bugs.

Definitely not a bedbug. It is a weevil, family Curculionidae. A beetle, and not normally found indoors. It looks a bit like Baris, but I cannot tell from the picture. https://en.wikipedia.org/wiki/Baris_(weevil)

great, thanks! The Weevil type looks definitely right. Not sure about Baris though, it looked a bit more like one of these Lixus Junci https://en.wikipedia.org/wiki/Weevil#/media/File:Lixusjunci.png (the picture i provided doesn't really give a lot detail, sorry)


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(Reference request) Formal abstract theory of evolution?
EDIT: please feel free to suggest books that are the closest you can come up with to what I'm looking for, even if it doesn't exactly overlap!
I am very well acquainted with the theory of evolution as informally taught. E.g. I don’t need a book that explains the theory, or refutes popular misconceptions.
Instead, I am looking for a formal theory of evolution as a process, and I am not specifically interested in the biological aspect of evolution, but in evolution as a more generally occuring process.

How do we formally state the different assumptions of Darwinian evolution? (Random change, heritability, natural selection).
What happens if we change these different assumptions? (Non-random mutation? Maybe, selection criteria that are influenced by the mutations, rather than independent of it)
Are there quantitatively different results of evolution based on these assumptions?
Something I find very interesting: What kind of non-biological evolutionary processes can we describe formally? E.g. evolution based on some form of non-random mutation, or based on different types of heritability. What are the different implications of different formal assumptions. How do these differences apply to different evolutionary systems? (E.g. evolution of ideas, cultures, computer viruses, evolutionary algorithms).

In summary, I am looking for a book that introduces in a very abstract way the properties of evolutionary systems (does not have to be focused on biological evolution. I’m interested in the formal properties of such systems).
NOTE: I am NOT asking about a book on modelling highly specific processes that apply to specific biological systems, such as population dynamics of preditor-prey relations. I’m interested in general, abstract theoretical analysis of the notion of an evolutionary process in general.

This question is quite wide i hope you will get answer.

@L.Diago, but someone could give me SOME suggestion, without necessarily giving me everything I’m interested in, right?

[Thomas Cavier-Smith] (https://en.wikipedia.org/wiki/Thomas_Cavalier-Smith) had interesting idea about inheritance in clay. But this theory have never been proved/ disproved (some guy tried to do something like that but not with clay). I am not quite sure how the influence selection would look like.  But if non-random mutation exist i thing the specious wont  be able to adapt to their

enviroment effectlivly on the other hand you technicly can be a X-man in world of non random mutation. So in our world all mutation is random but there is some region which can be more mutated then others part of DNA. Others non biological evolution system is for example you languages systems. I hope i tell you something what do you really want to.

@L.diago, note that non-random mutation doesnt mean NO mutation. It just means that there is some directionality to the mutation. For example, I've heard it argued that businesses evolve according to a kind of non-random mutation. But yes language evolution s another example! I would like a book on the formal properties of such evolutionary systems. If there is no such book, any book that is somewhat like it would be welcome as well!

I didnt say no mutation, but mutation which wont be random..  The randomness is what life makes soo well adapt on diffrents enviroment..

If you are interested in non-biological evolution then you may be interested in artificial evolution and simulated evolution. .

Each of your bullet points could be a full question in and of themselves, as it is this makes the question way to board. You  will be better off asking separate questions, especially since several points are unclear or erroneous. .

@John, but I am not asking for answers to those questions... I am asking for a book on the topic that encompasses these questions. Also, what is erroneous?

You will not find a single book covering such a broad range of topics, Again you would be better off asking the questions separately, especially given how vague your criteria are.

@John, I'm pretty sure that given the responses, the think I'm looking for either doesnt exist or is not well-known. I think this question should be closed

neither is the case you are simply asking for too much from a single source. Each bulleted point would come with recommendations for several books or hundreds of papers. Or you could simply ask the questions you really want and let the answers lead you to sources.

@John, perhaps it is better if I first try to get an overview of which sub-fields in evolutionary theory there are, and what they study, then I might be able to ask a more pointed question.

Perhaps this would be a good way of stating it: I am interested in a rigorous mathematical introduction to generalized Darwinian mechanisms

@Programmer2134 then you will (mostly) find it in the books that have already been mentioned. Although I should note that the generalization of population genetic principles to macroevolution is still contentious and an area of active research.

@NatWH, I'm not sure why you mention macroevolution?

Because not all of evolution has been satisfactorily mathematically formalised :P

you may want to look at the field of "adaptive dynamics" for a more abstract look, the most detailed mathematical explorations will be tied directly to genetics.

@John yes that is closer to what I want. The more abstract the better. I don’t want details.

The theoretical framework that best fits the kinds of questions you have in mind is evolutionary game theory.
The foundational text is perhaps Maynard Smith's Evolution and the Theory of Games, but I'd recommend one of the standard textbooks instead, say Gintis (2000), Game Theory Evolving or the more advanced Hofbauer and Sigmund (1998), Evolutionary Games and Population Dynamics.

Summarizing evolutionary processes to game theory is, IMO, border-line  ridicule. Of course evolution of social behaviour do matter but in no way can evolutionary game theory be seen as the core principle of any thin one would want to call evolution. Typically, I don't think game theory is being used in evolutionary algorithm at all.

Evolutionary game theory applies to any and all evolutionary processes. It is not tied to social behavior in any interesting sense.

From wikipedia : Game theory is "the study of mathematical models of conflict and cooperation between intelligent rational decision-makers". Its application to evolutionary processes as well as Hamilton's extension by including a relatedness term are fundamentally limited to the study of the evolution of interactions (conflict, cooperation, etc..) among agents (aka. social evolution).

Evolutionary game theory precisely forgoes the assumption of rationality in favor of evolutionary regimes. The interactions and conflicts in EGT usually just codify differences in fitness between, e.g., a base phenotype and a mutant.

Difficulties in your question
It is a little hard to know exactly what you're after because 1) the question is broad 2) some concepts you talk about are a bit unclear.
For example, by 'random change' I suppose you mean genetic drift but I am not sure. The term 'random mutation' is a little undefined (see this post). You list 'Random change, heritability, natural selection' as a list of assumptions (at least I think you mean those are assumptions) but those are typically not common assumptions of evolutionary models. Also, the list is not in any way intuitive, so it is unclear what you mean by it. The phrasing "selection criteria that are influenced by the mutations" is also very unclear. Of course, selection, by definition, is dependent upon the genetic variance.
From our discussion in the comments, I think you are attempting to group different fields under a single concept just because they have the same name. But it is not because they have the same name that they are governed by the same basic principles. For example, it is not because the concept of plasticity exists in both biology and physics that these concepts are in any way related and that there is a general theory of plasticity that encompass both fields.
Evolutionary genetics
That being said, you could gain from any good intro textbook to evolutionary genetics. I especially recommend Population genetics, a concise guide. You will find more such recommendation in the post Books on population or evolutionary genetics?.
Evolution of ideas, cultures, computer viruses, evolutionary algorithms
In your last question you mention 'evolution of ideas, cultures, computer viruses, evolutionary algorithms'. I think you are referring to these concepts so as to clarify that you are not so much interested in the biology of specific organisms but really into the process of evolution. I do not recommend starting reading about these concepts before having a background in evolutionary genetics. You might otherwise make the mistake to over stretch an analogy.
Note also that the field of memetics (evolution of ideas, cultures) is a young field in which very little empirical testing is possible. So, I don't think it is wise to start there if your goal is to increase your understanding of evolutionary biology.
In any case, I am not able to suggest a good book in any of these fields (Evolution of ideas, cultures, computer viruses, evolutionary algorithms).

see my answer, I'm guessing those parts that are less clear come from fusing ideas on natural selection, Hardy-Weinberg population stuff, and neutral theory. In which case I think the related monographs should clear it up. Just throw up your favourite evolution books! I would love to hear them as well.

"by 'random change' I suppose you mean genetic drift but I am not sure." No I simply mean mutation of individual genes. "In your last question you mention 'evolution of ideas, cultures, computer viruses, evolutionary algorithms'. I think you are referring to these concepts so as to clarify that you are not so much interested in the biology of specific organisms but really into the process of evolution." No that is not the reason why I mention it. I mention it because I am specifically interested in the process of evolution in general, not just to organisms.

By "evolution" I mean the general process that occurs roughly whereby (1) there is a sequence of "samples" from a space of possible elements (e.g. a sample from the space of possible DNA sequences, where each such sample is a "generation" of individuals), and where each sample is determined as a random deviation from the previous sample (previous generation).

@NatWH I've listed books I like in the linked post Books on population or evolutionary genetics?. My worry with suggesting a book like The Neutral Theory of Molecular Evolution is that it is not introductory and the OP might have a hard time reading it. I have never read Gould and Lewontin so I can't comment on these books.

By "random", in this case, I roughly mean: "independent from the other factors in the model". Though I didn't intend to specify randomness very precisely, as my goal is not to get a specific answer to these points, but to get a general introductory book about these topics

@Remi.b that is very fair. That's why I put Futuyma in as the start of my suggestions.

@Programmer2134 Such concept of evolution encompass many different processes. One should not make wrong analogies from one field to the other. You won't find a good book that talk about all these very different types of evolution. Note that you will need to understand the existing models before trying to investigate violation of their assumptions.

I think population genetics is not exactly what I'm looking for, as it seems to be quite specifically biological (in the sense that it goes into the specifics of the biological mechanisms behind the relation between genetic an phenotpyic traits for example), and therefore not very applicable to say, evolutionary algorithms in intelligent computing.

@Remi.b, I'm not sure what "wrong analogy" you're talking about, but ok....

Again, I'm looking for a formal theory of these different processes. it is possible that this simply doesn't exist yet. (I am not interested in empirical testing, or in understanding how biological evolution happens in the real world).

Of course, they exist. The book I suggested (as well as Kimura's book NatWH suggested) are all about modelling. There is no mention of specific species. It will teach you how to compute expected heterozygosity after n generations of drift and selection and other stuff of the kind. Generally speaking, there is a lot of math in evolutionary biology, more than in most other fields of biology.

@Remi.b you clearly don't understand that I am not interested in specifically biological evolution, despite me repeating this a few times now. That is, I'm not interested in specifically genetic/biological factors such as heterozygosity, etc. I'm interested in the more general process of evolution, e.g. as applied in evolutionary algorithms for computer programs, etc.

@Programmer2134 most evolutionary algorithms will be founded in at least some way in fundamental evolutionary math. However, I suggest that biology.SE might not be the best place to ask if you're looking for things that veer into algorithms in machine learning...

@NatWH, It seems I'm in the wrong forum, yes... (though I'm interested in theory, not specific algorithms. But nevermind) I'll wait for some more responses, but otherwise I think this question should be closed

@Programmer2134 I think you are attempting to group different fields under a single concept just because thy have the same name. For example, it is not because the concept of plasticity exists in both biology and physics that these concepts are in any way related and that there is a general theory of plasticity that encompass both fields.

@Remi.b, let's just agree to disagree. This is not going anywhere

@Programmer2134 I can agree with that :D Good luck!

As a body of literature, that covers quite a broad range of topics that have been discussed at length in many, many papers. Of course, you might find something out of a broad-level textbook (I suggest Futuyma's Evolution). You might also enjoy Kimura's The Neutral Theory of Molecular Evolution (although be aware of its follow ups and critics), and its (somewhat) ecological counterpart, Hubbell's The Unified Neutral Theory of Biodiversity and Biogeography. There are loads more, but this might be a good starting point.
EDIT: also Gould's The Structure of Evolutionary Theory, and Lewontin's The Genetic Basis of Evolutionary Change.
EDIT: also, not directly but since I have just finished reading it: Simpson's Tempo and Mode in Evolution. This is mostly from a palaeontology perspective, but it brilliantly preempts several arguments about rates of phenotypic evolution, individual vs population processes, and the asymmetry between mutation and substitution and what that means for evolutionary biology.

Add in several of Dawkins books (selfish gene, extended phenotype, and climbing mount improbable) which will dive into basic assumptions, artificial evolution and provide a counterpoint to Gould.

@John I would classify most of those under things OP would already have read, given the intro to his question. Dawkins is one of the most well-known popular science authors after all. Also bringing in some Dawkins necessitates bringing in some E. O. Wilson...

I make no assumptions about what the OP has read since they seem unclear about some of the basic tenets of evolution. And of course asking about non-biological evolution always makes me think of dawkins work on virtual/simulated evolution and ideas about memetics.

Eh, I've voted it be closed, anyway. You're right that it is far too vague, and appears to be more about machine learning.

@John, purely out of curiosity: what basic tenets do I seem unclear about?

random mutations are an assumption of evolution, that mutations are statistically random is an independent conclusion and not necessary for evolution, mutation is not even really necessary for evolution it just will not occur for very long without it.

@John, lol ok. I didn’t say any of those things, but let’s just stop this discussion, because this isn’t going anywhere.


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Do Scrubjays weigh peanuts by picking them up?
I have been feeding scrubjays where I live (Monterey, California) with peanuts in the shell.
Something interesting I've noticed them do is, after I've laid out a selection of peanuts for them, they pick them up in their beaks and seem to be determining which one they want to fly off with. I have seen them first eye them all for a couple of seconds, then pick one up, shake it in their beak as if listening or "weighing" it, then picking up another one, or even three, and then going back to one of the previous ones and flying off with it.
What are they doing? Weighing them? "Counting" how many nuts are in the shell? Listening for something?
Here is one "in the act":

I doubt anyone knows the answer to which aspect of variation jays are considering when sampling nuts (although my guess would be mass). Langen (1999) did do experiments that explored the sampling behaviour you've noticed — they offered jays samples of peanuts with ranges as wide as 1 g (i.e. over a range from 1 to 2 g). The analysis mostly focused on when jays would be choosy (lots of nuts vs few nuts available; low vs high variability; competitive vs non-competitive scenarios; subordinate vs. dominant individuals; etc.)
Jays were reasonably accurate at visual assessment (the first nuts they sampled were statistically significantly heavier than a random sample of the available nuts), and their subsequent sampling behaviour (what you're observing) further improves their success in selecting heavier-than-average nuts:

Jays improve their accuracy at selecting a high-quality peanut via the initial visual scan and the subsequent sampling behavior. Peanut sampling (using the beak to handle several  peanuts  in  succession)  results  in  a  higher  rate  of food  storage  than  is  attainable  by  simple  visual  inspection, at least when options are not too similar.

In order to figure out what aspect of the nuts birds are actually assessing, you'd have to do experiments where you found a way to independently vary the number of nuts, mass, sound of the nut when shaken, etc., and see what happened.
Jablonski et al. (2015) actually did experiments with Mexican jays (Aphelocoma ultramarina) to evaluate proximal mechanisms of nut choice, and suggested that they do use auditory cues — but the authors don't actually show any tests of auditory cues:

(abstract) Jays evaluated each peanut by performing fast movements of the head combined with additional fast movements of the beak, which may open and subsequently close producing sound at the moment of hitting the shell. These movements seemed to provide Jays with additional sensory information that led to a more strict discrimination against non-preferred peanuts. ...
(discussion) We are now analyzing a series of experiments that seem to indicate that sound is indeed taken into account by Jays handling the peanuts and that it may be more important than the perception of heaviness ...

If these subsequent analyses were ever published, I haven't been able to find them online ... if you were really interested you could contact the authors and ask them ...
For what it's worth, there is also a paper titled "New Caledonian crows infer the weight of objects from observing their movements in a breeze" ...
Again, my guess would that the jays are 'weighing' the nuts. Mass should be pretty easy for them to assess, and closely related to the energetic/nutritional reward given by a particular nut.

Langen, Tom A. “How Western Scrub-Jays (Aphelocoma californica) Select a Nut: Effects of the Number of Options, Variation in Nut Size, and Social Competition among Foragers.” Animal Cognition 2, no. 4 (December 3, 1999): 223–33. https://doi.org/10.1007/s100710050043.
Jablonski, Piotr G., Sang-im Lee, Elzbieta Fuszara, Maciej Fuszara, Choongwon Jeong, and Won Young Lee. “Proximate Mechanisms of Detecting Nut Properties in a Wild Population of Mexican Jays (Aphelocoma ultramarina).” Journal of Ornithology 156, no. 1 (December 1, 2015): 163–72. https://doi.org/10.1007/s10336-015-1193-6.


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Can herbs absorb harmful substances leached in water supply
I have small herb garden (parsley, coriander mint and basil) that is watered from below by a hydrophilic filter using capillary action from a reservoir. This filter allows water soluble nutrients to be fed to the herbs.
The manufacturer of the filter use a special propitiatory additive in the filter that allows for excellent water flow. I need to know the the harmful implications of the material as they have stated the unknown "additive in the filter is not FDA approved". They will not tell us what additive is to protect their intellectual property.
My question is that will the herbs absorb the additive regardless assuming the additive is leaching into the water. Say that 1 ppm (parts per million) of substance X is in the water. Will the herbs absorb that and propagate it to their leaves. If so how much of the substance? (very rough estimate will do)
TIA, Dave

You'd have to test it. Plant roots naturally pull poisons like heavy metals out of the soil through water. These are called metallophytes, and can even be classified into what're called hyperaccumulator plants. The use of plants to remove harmful substances from the soil, air or water is called phytoremediation.
The process of absorbing harmful substances, however, relies on the structure and size of the substances involved because the substances must enter cells. We know from elementary biology that cells only allow molecules of certain properties to pass their cell membranes. Since the filter additive in question is an unknown, it's hard to say if a plant would absorb it. It's also hard to say if it's harmful to you, or if it even gets into your water. Testing for a chemical of unknown behavior requires some analysis like mass spectrometry (fair example).


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Is happiness or pleasure an evolutionary programming for survival?
I think that whenever we feel some kind of happiness or pleasure it is always related with improving our chances of survival, that might be temporarily or in long term, might be of only of an individual or his/her relatives or all human beings or all living beings as a whole.
I find that a sense happiness or pleasure is linked with the survival (might not be true as it's based on personal observation).
 We crave for things like attention & being cared, beauty & physical health, power (& money). Attaining them gives us a sense of pleasure, and these things improves the chances of our survival. People having power & money dont die out of scarcity. People having beauty & physical health get to pass their genes more often(keeping whole human history in mind). Dogs developed their behaviour around humans so as to get more attention & care thus improving their chances of survival. We also feel happy helping other people, we feel happy making more friends.
  But there is no simple answer to this one as we also have tendencies to hurt ourselves and some people derive pleasure in hurting others.
So is pleasure or happiness evolutionarily programmed into us to better our chances of survival?

"Evolution" and "programmed" together sounds a bit strange.

Please do not post to this site as a new user without consulting the help to find out what the scope of the site is and what sort of questions are acceptable here. This sort of question based on a "feeling" and asking for answers that can only be subjective are off-topic and a waste of everybody's time.

@David I fail to see how is this a subjective question. Please let me know where I made the mistake.

Describe an experiment or study that would provide an objective answer to your question.

I don't know of any experiment as such but there is definitely a correlation between pleasure/happiness and our improving chances of survival

Look at the things we crave. Being caref or loved, getting attention, power, having beauty/physical health. All these give us some sense of pleasure when we get them. Why so? When we help others why do we feel good? So my question is that does improving our chances of survival the cause of our happiness or pleasure.

Please @ me in if you reply to my comments. This is a scientific site. Statements like "there is definitely a correlation…" without citing any research in support is scientifically worthless. And as you devote your following comment to arguments in favour of this idea it would appear that your question is not an attempt to test it with scientific evidence but to solicit others of like mind to say "yes you're right".

@David I have no problem if you think my question is unscientific. I don't know the standards used to measure the worthiness of a question, and I believe such standards (if exists) are mostly subjective. I was thinking about the reason why we feel pleasure and happiness and couldn't figure anything  more than this. I don't belong to the field of biology and couldn't find any research or experiment related to it. The purpose of the question was not to put forward what I think to be true rather to know where I am wrong. And for that reason I am totally open to discussions and criticism.

Our current understanding is that pleasure is one of the major ways your brain gets "you" to do things, it is the basis of positive reinforcement of behavior and associative learning. It can almost be thought of a a tag for an individual behavior that says "do this again/more". That pleasure alone can motivate animals to do things has been understood since way back in the Skinner box experiments where a wire to the pleasure center was inserted in rats and said rats would keep doing whatever behavior they associated with stimulation via the wire foten to the exclusion of all else. The basis of our learning could be summed up as do things that elicit pleasure, don't do things that elicit pain. tying many complex behavior to a single signal seems to make it easier to control and even prioritize very complex behavior, just do whatever yields the most pleasure, of course humans and many other animals have many more competing emotions and other factors, like metacognition. But for simpler animals it is easy to see how this system is efficient, it is easy to tag new behaviors or experiences into this system, at its simplest form just connect (possibly inhibitory)a few neurons triggered by the behavior or memory of the behavior to the pleasure center.
Of course it is not perfect, few things that evolved are, behaviors that are not beneficial can trigger the system, especially novel or extremely rare behavioral options, especially ones created by technological advancement, drug addiction being a great example. Evolution is very poor at preparing organisms for novel conditions like the modern technological world. And the our brain did not evolve under conditions where cocaine (as an example) existed. Just because something is pleasurable does not mean it is beneficial.  The full range of behaviors that can elicit pleasure would be well beyond the scope of a single question but it is quite clear pleasure itself is an evolutionary advantage, it is one of the major reasons we learn to eat, drink, reproduce, and make social connections.
Happiness, is more difficult, mostly because it is a poorly defined term in biology, it is unclear if it is distinct from simple pleasure.

All features of life have evolved in order to better the chances of reproduction, the feeling of happiness is included.  After all, happiness is just the release of various molecules such as dopamine, oxytocin, and endorphins, that cause the body to more likely produce a certain behavior.
These chemicals can produce advantageous behaviors by promoting deep friendship, mating bonds, and gratitude in an investment paid-off.  However, they can also provide bad behaviors if jealousy or laziness emerges.  All emotions exist in a tug of war in evolution, in fact Darwin wrote a book entitled: "The Expression of the Emotions in Man and Animals".  While I have not read all of it he probably states how fear, jealousy, anger, etc. all can promote both good and bad behaviors.
More recently, scientists have tried to study specifically the evolution of happiness two publication are by Nesse and Buss.  Both are not very sure, but note the evolutionary advantages of evolution.
So the short answer to your question is yes, with the caveat too much, or too easy a sense of happiness has its downsides, and that all other emotions and measures of the body are effected by evolution.

All features of life have evolved in order to better the chances of reproduction This is wrong. It is too a panselectionist view of evolution. You might want to summarize the two papers you linked to, they are probably of interest. I would love an answer that highlights the difficulty to define the concept of happiness and how much it may be culture specific.

Yes I generalize evolution and remove the random aspects, but if natural selection is not selecting for features that enable better reproduction then what is going on?  Also an answer that branches into cultural aspects would appear an anthropological answer, not a biological one.

Your arguments amount to an assertion of belief, and as such have no more value than those opposing ones based on religious beliefs. Indeed they are worse as they purport to be scientific but are actually anti-science.

My answer is about belief?  I try to cite chemical pathways, Darwin, more recent work, and generally give an answer that is not very confident but based in logic.  If you have a problem with my answer, then please point to it, but don't just say I am anti-scientific outright with providing any supporting feedback - it is not helping anyone, and instead insulting.

You might be better off saying "pleasure and the brain reward system is too widespread an adaptation to not expect an evolutionary advantage". not every feature organisms have are evolutionary advantages. An actual sourced description of the system would also be a big improvment, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4491543/


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Is this a worm or snake?How to get rid of it?

Hi! I found this thing in my bathroom. I killed it but still it's friends keep on reappearing. It moves slowly , is it a snake? How can i get rid of them? I live in Mumbai, India. It's rainy season here and the size of animal varies from 5 cm to 15 cm approximately.

This animal moves slowly. Have a look at this video https://youtu.be/IDhxsmuRq3w

If it's dead you should be able to get some closer pictures? (Looks to skinny to be a snake, but really hard to see anything)

Hi! I just got a clear video of its young relative. Can you tell me what is it? https://youtu.be/gOsNf-jtppM


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How to determine the number of parameters in a phylogenetic model?
I want to calculate the AIC for a phylogeny that I inferred via maximum likelihood. To calculate the AIC I need to know the number of parameters in the model. But how do I determine this?

Biostar forum... bio informatics forum is a popular place which specializes in phylogeny statistics data researchers questions and answers https://www.biostars.org

The number of parameters depends both on the number of taxa and model of sequence evolution. The topology is not typically considered a parameter in the usual sense of statistical inference (as it is the a priori specified topology the likelihood was calculated on).
So, for example, if you infer a tree from nucleotide data for 25 sequences under the General Time Reversible (GTR) model with gamma distributed among-site rate heterogeneity and empirical stationary frequencies (this is commonly called GTR+F+G), then you would have 56 parameters with the following breakdown: 2n - 3 = 47 branch lengths (where n = 25, the number of tips), 3 frequencies (because these sum to 1, once three are known the other is automatically known, so we only count 3 estimated parameters), 5 substitution rates (there are actually 6 substitution parameters in GTR, but it is typical to set one, usually G > C, to 1, and estimate the others relative to this, hence only 5 estimated) and 1 alpha parameter for the shape of the gamma distribution of rates (gamma distributions actually have two parameters, alpha and beta, but for phylogenetics we usually constrain them to be equal).
In total, this gives 47 branch lengths and 3 + 5 + 1 = 9 model parameters, and 47 + 9 = 56

Thank you, @NatWH! This is extremely helpful. In any of the phylogenetic classes of objects in R (e.g., phylo) is there a way to extract the number of parameters?

I don't know - R objects of class phylo don't store model specifications, so I doubt it. But there may be a function somewhere. If not, it should be simple enough to write your own.


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ELI5 what is true breeding?
In "Variation under Domestication", Darwin makes several references to the concept of true breeding:

They believe that every race which breeds true, let the distinctive characters be ever so slight, has had its wild prototype.

And:

I crossed some white fantails, which breed very true, with some black barbs.

Before diving into the book, I never heard of the term, so I looked it up and found this definition in the Wikipedia article on Zygosity:

A cell is said to be homozygous for a particular gene when identical alleles of the gene are present on both homologous chromosomes. The cell or organism in question is called a homozygote. True breeding organisms are always homozygous for the traits that are to be held constant.

But this is rather technical and it's not the kind of explanation I would give to a child.
What is true breeding, in simple terms? When is breeding not considered true?

In the context of Darwin's Variation under Domestication, "true breeding" is a phenotypic characteristic rather than a genetic one.  True-breeding organisms produce offspring that are identical to themselves, concerning some trait -- i.e. white fantails, when bred with white fantails, produce characteristically white offspring.  For diploid organisms, true-breeding typically implies that the parents are homozygous at the locus conferring the trait of interest.

Case A: Not Breeding True
If you cross-breed two random dogs, the offspring are likely to only vaguely resemble either parent.  If you could clone a random dog to obtain two genetically identical dogs with different sex, you would likely still only get offspring that vaguely resemble their parents, because the chromosomes of the parents would come in pairs composed of chromosomes from the grandparents; but which grandparent contributed each chromosome in the offspring would be random.  There is of course a very small probability that an occasional puppy would be identical to its parents — about 1 in 278.
Case B: Breeding True
On the other hand, if both chromosomes in each pair were identical for both parents (a situation that can be approached via a long series of inbreedings and selection, or could probably be obtained artificially in the lab), all the randomness would be eliminated and the offspring would be identical to the parents, if we neglect the likelihood of mutations and other genetic novelties.
So, in fact "breeding true" is just one end of a spectrum that is determined both by the amount of similarity between the parents' genetics, and by the amount of homozygosity in each parent.  This whole concept goes right over the head of the majority of adults, so getting it across to a child could be a serious challenge.  So to simplify: "Breeding True" means that the parents are identical and all the kids are identical to the parents.  It happens only very, very rarely.

In farming, "breeding true" is common. For example, "heirloom" plant strains are almost always ones that have been inbred for many generations to the point where they "breed true".


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Modern understanding Darwin's "correlation of variation"
In Variation under Domestication, Darwin makes several references to the concept of "correlation of variation":

I will here only allude to what may be called correlated variation. Important changes in the embryo or larva will probably entail changes in the mature animal.

And:

Some instances of correlation are quite whimsical; thus cats with blue eyes are invariably deaf.

In the chapter's ending, he also calls this "correlation of growth":

Variability is governed by many unknown laws, of which correlated growth is probably the most important.

I gather that this is Darwin's humble way of admitting that there are many unknown unknowns, at least as far as correlation is concerned.
But, since 1859 until present day, what did we find out about this quirky aspect of evolution? Are all cats with blue eyes deaf?

It seems obvious: one characteristic or change is associated with another, as with blue eyed cats being deaf.

Yes, I was more curious about the modern understanding of the topic, that is, if the theory is as sound as it was perceived back then and, if not, in what regards.

One must not confound a phenotypic variance-covariance matrix (usually called $P$) and a genetic variance-covariance matrix (usually called $G$) for a set of phenotypes. The mutational variance-covariance matrix is also a common concept (usually called $M$). There are a lot of papers on the evolution of the G-matrix (and related matrices).
In the abstract of Roff (2000), you can find the equuation
$$\Delta\bar z = GP^{-1}-S$$
, where $\Delta\bar z$ is the vector of mean responses, $G$ (often just called the G matrix) is the matrix of additive genetic variances and covariances, $P$ is the matrix of phenotypic variances and covariances and $S$ is the vector of selection differentials.
You will find much more by just googling "evolution of G-matrix"

It might be helpful to add a lay summary to this answer, since I think it's on a bit of a different level than the original question.


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Has Epipremnum aureum lost its ability to reproduce sexually?
In this recent question the shy flowering nature of Epipremnum aureum (Golden Pothos) was discussed:
Where can I find a picture of the inflorescence of Epipremnum aureum (golden pothos)?
To summarize: (1) The two first and only observations of the plant flowering date back to the 60s and (2) genetic analysis yields a potential explanation for why the plant is so rarely flowering
Question: Is this sufficient evidence to conclude that E. aureum has lost its ability to reproduce sexually?
(Triggering thought: It is very unlikely that two specimens flower simultaneously, at a distance from each other that allows pollination, that pollination actually takes place and that the seeds germinate and successfully grow into new plants)


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Insect identification - is it a bed bug?
We were on holiday and got bitten by (most probably) bed bugs. We then carried them home, and I also saw a typical one: 4mm, flat, round, black. I thought it was pretty clear we had bed bugs. I smashed one:

Currently (2 weeks later) we have a lot of small insects in the house, like shown in the picture. But they don't really seem like bed bugs, do they? The big ones look like bed bugs, but the small ones don't?
What is it? It's around 2mm (others are much smaller, very tiny, less than 1mm). They can jump (or run really fast) 2cm if I try to squash them with a finger.

Update:
The small one is very similar to a psocid?!
Update 2:
They have wings.. I think they're psocids.
What I also realized, I probably have two different larves. I take some more probes..

Top photo looks like a bed bug. Bottom one looks very much like a psocid.


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Molecular Docking Enzyme Inhibitor Biosensor?
I had some task to study Molecular Docking relations with Biosensor and I am really new with this discipline (beginner). I am docking C60 with Glucose Oxidase and my question is: what would happen if C60 inhibited the active site of enzyme? Can the protein still be used by the biosensor or would it be broken because of the active site used by C60?

(1)C60 is fullerene nanomaterial; (2)Actually c60 is "mediator" to glucose oxidase in real application biosensor. So in simple ways when glucose oxidase meet the substrate. It will made product which can be detected by c60 and c60 will transfer electron to electrode and convert from chemical to electrical energy. What i confused is how interaction happen between glucose oxidase and c60. If c60 inhibit in competitive then the enzyme cannot be used. Or inhibit in non competitive still enzyme cannot be used.

So if i docking with AutoDock Vina and get energy binding (Gibbs's free energy) -12.0 and -8.0. It's mean -8.0 better than -12.0? Because -8.0 have smaller energy binding which made weak inhibition than -12.0?

Okay thats soo helpful logic, i also read about enzyme immobilization before the enzyme attached to biosensor. Is enzyme immobilization make the enzyme rigid? Which mean non-competitive cannot change its structure?