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Bifurcation is a fascinating concept found in various fields, including mathematics, physics, and biology.
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In ODE cellular models of cardiac electrophysiology, look for examples of early afterdepolarizations and cardiac alternans. These have been long investigated from the point of view of bifurcations.
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The framework of economics today draws largely from post-War scholarship. And here, we remember the use of biomathematics by Paul Samuelson and contemporaries of the sixties and seventies. Now, that framework has been challenged and partly because of its finite dimensions. Hark back the 2007/8 crisis. Take ‘forward guidance’. It terrified the central banker. The models could not handle the realities of strongly nonlinear dynamical systems. Another crisis is here, Covid. Looking ahead, economics might have to draw more from the data-driven linearisation of engineering. And the Koopman world comes to mind. So we must ask, why can’t engineering and economics merge? And the question is more relevant in the most strongly nonlinear spaces of the lower income countries. Do you see the joy in dropping on a university hill of Africa and being welcomed by a department of engineering and economics? We just have to overcome a few institutional issues (norms and values). And the jolt of Covid should help us overcome the institutional challenges.
The wisdom of the early twentieth century established institutes of advanced studies for deep interdisciplinary work. The lower income countries don’t have those institutes. And it seems institutes in the advanced economies have lost their original fervour. So, the merger seems the most feasible solution for economics.
PS: And to Koopman people in their corner, this note provokes augmentation for transients.
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Think of the conceptual power of Black-Scholes-Merton equation. Stay with the PDE, don’t rush to the solution. It seems criminal that students of financial economics should be kept away from engineering students - BSM captures the richness of the heat equation. Yet let me tear myself. It seems criminal that graduate education is not presented as a subject of physics. If anyone doubts interdisciplinarity, peer into BSM. Now, as we solve the PDE, quadratic variation emerges. To talk public policy without quadratic variation is just empty. And we are back to interdisciplinarity. We might with a department of engineering and economics.
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A  phase transition of order k is mathematically characterized by a loss of regularity of free energy f: f is k-1 differentiable but not k differentiable. There are many examples of first and second order phase transitions in experiments and in models. There are also cases where f is C^{\infty} but not analytic (Griffith singularities).
But are their known example of phase transition of order k, k>2 ?
A third order phase transition would mean that quantities like susceptibility or heat capacity are not differentiable with respect to parameters variations. But I have no idea of what this means physically.
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Dear Prof. Bruno Cessac, in addition to all the interesting answers in this thread, there is a paper that explains historically the evolution of the Ehrenfest classification of the phase transitions, it might be good to add it since it talks about the Pippard extension of the classification when there are singular points in the specific heat at the Tc as in the ferromagnetic/antiferromagnetic-to-paramagnetic transitions in Ni (ferrom.), MnO (antiferrom.) and other crystals.
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In the context of complexity, it is well known that each change that is given to nodes or relationships in a network will give emergent properties, and I am looking for a way to model these effects.
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Thank you. There is one crucial aspect to complex systems that you probably already know but it is important to repeat it again and again.
Entropy.
The concept entropy enables us to measure the operational state of any complex system in existence without having access to its totality.
It is possible to observe just one signal generated by the observed system and from this signal -- using entropy measures -- to assess the operational mode and other properties of the observed CS.
I did propose and used the same approach to predict ventricular/TdP arrhythmias from ECG recording (signal) of the heart (CS).
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I tried to find that and no way, It is required to construct your own code.
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I would like to calculate dissociation constant (Kd) using fluorescence anisotropy.
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1. Plot fluorescence anisotropy versus substrate concentration [A] for the protein. You will have a maximal value (y1) to which the data extrapolate and a minimal value (y2). Maximal and minimal values do not necessary correlate to bound or unbound forms. Whichever one happens at higher ligand concentration corresponds to the bound form and whichever one happens at lower concentration corresponds to the unbound form.
a. If the data can be fit to a fraction bound (Xa) equation, do so. The fraction will be calculated as follows:
Xa = {e^(-nH*(Kd-[A]))}/{1+e^(-nH*(Kd-[A]))}
nH is the Hill constant, a measure of cooperativity. It will be “1” if the data is not cooperative, between 0 and 1 if there is negative cooperativity, and no larger than the number of binding sites if it is infinitely cooperative.
b.Then the intensity can be mapped to this fraction bound through the maximal and minimal values of anisotropy:
anisotropy = y2 + (Xa*(y1-y2))
Use the plot of intensity versus concentration and non-linear regression fit of the data to determine the value of Kd for the ligand. When your fit matches the observed data with a minimal chi-squared value, you have the correct value of Kd.
One more thing that may help: you have to put in initial parameter guesses for nH, Kd, y1 and y2 when you do it this way. You may find that setting the Hill constant =1 for your first guess and NOT floating it during the non-linear regression speeds your mathematics up and lets you determine close guesses for the other parameters faster and with greater accuracy. The same would be true if you fixed y1 or y2. The fewer things you have to vary in this calculation, the more reliable your results will be for the rest. It's kind of like having to reckon the position of the sun into a determination of direction you are travelling, and rather than having to calculate the direction of the sun, you just point to it because you know where it is. See if you can get the fit to converge onto your data without having to float all four parameters. If you can, then you should go with that.
Oh, and sometimes the fluorophore will not respond to the binding of ligand, as observed by no change from the maximal and minimal values of anisotropy. In such cases, you cannot use fluorescence to determine ligand binding.
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Dear all,
I am staining two adjacent cellular structures solids with fluorescent antibodies (Alexa-488 and 555). I want to calculate the coverage of the small solid respect to the big one.
In disease state, they both reduce their volume although is more dramatic in the small one.
I know volume ratio is not enough nor surface area.
Could you suggest me any help?
Best regards,
Alan
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Hi Katherine and Ammar,
These structures are approximately separated by 30-50 nm and they are imaged in 50-60 um Z-stack in a Confocal microscope (40x). So, by fluorescence staining we can easily differentiate them. Volume, surface area and any other morphological analysis are carried out in Volocity.
Lets put the example of the inner and outer mitochondria membrane. Let also says the inner membrane degenerates more in a particular disease than the outer one. How can I calculate the degree of lost of coverage (or denervation as happen in synapses) or contact between them?
I can plot reduction in size independently (volume, area, perimeter, surface, etc) but this does not represent the parallel loss.
- I thought the surface area may help, but this is a measure of the area of the external faces of each structures but not of the internal one (They are 3D structures).
- Also thought that I can analise the colocalization value (Pearson and/or Manders) but that does not give me the loss of coverage of the small structure respect to the big one (inner membrane vs outer).
- Everything may be easier if these were 2D images, as I can calculate the difference in area. Here they are 3D solid with irregular shapes.
Hope this makes it clear.
Thanks in advance!!
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I have some individual interest to understand a little bit more these two phenomena, because the apparent mathematical similarities between them, and because some particularities, too. The overview to direct possible concerned researchers to solve this question can be seen in the attached link. Thanks for you interest.
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This is better explained here
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I am calculating the correlation values between two data sets of size 257. I want to know what is the critical value of correlation for a sample size of 257. I tried searching on the web, but critical values corresponding to 100, 200 and 500 are seen but not 257 specifically.
So, what is the formula to calculate the correlation critical value? There are a few online tools to calculate that, but I would like to know the formula so that I can integrate it into the code I am using so as to get correlation values along with the critical values.
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First of all, Ben Babcock's answer was awesome. I have adapted his R code to the t-distribution (so that you WILL get the same critical values as you see in the tables). I also managed to simplify it a bit, but ultimately this is just a modification of Ben's code.
critical.r <- function( n, alpha = .05 ) {
  df <- n - 2
  critical.t <- qt( alpha/2, df, lower.tail = F )
  critical.r <- sqrt( (critical.t^2) / ( (critical.t^2) + df ) )
  return( critical.r )
}
critical.r( 102 )
Thanks to Ravi for asking the question, and thanks to Ben for the code. Your answer really helped me out!
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Which tool is best for data plotting for scientific documents, journals, etc. In MATLAB, I did some plots with very low step size like the plot in the attachment, If I change different features like *, ^, v instead of '-' I am getting only thick lines (because of very low time steps). If I print in black and white printer, we cannot find the difference. How to overcome this issue. Can anyone suggest me a plotting tool to show the difference in black and white print out (we have to keep it in mind that we have to use very low time steps like 0.0005 also).
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Although the calculation be done with time step of 0.0005 s, the results are presented in time steps of 10 s, as can be seen in the attached plot. I recommend reduce the number of points to be plotted and then utilize dots, traces etc. of different colours.
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I want to know the method that determines the stability of dde for all situations.
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It depends of which kind of stability you want to investigate.
(i) Local stability => Search for singular points and then, linearize the system around these points
(ii) Global stability => Search for a Poincarré-Bendixon domain and/or a Lyapunov function
(iii) Lyapunov exponent is a quantity that characterizes the rate of separation of infinitesimally close trajectories, it is often use to ivestigate if the system is chaotic or not.
(iV) I recommend you the two book (The first chapter of the first book talk about your question).
A-
Mathematical Biology: I. An Introduction (Interdisciplinary Applied Mathematics) (Pt. 1) Hardcover
by James D. Murray (Author)
B-
Differential Equations and Mathematical Biology Hardcover – February 26, 2003
by D.S. Jones (Author), B.D. Sleeman (Author), D. S. Jones (Author)
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Organisation, its omni-presence, preservation and dependence, is possible the distinctive aspect of biological phenomena. Achieving a consensus about what is organisation and how can it be used to generate biological explanations would greatly benefit the development of (theoretical) biology.
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I Think you can find hints in René Thom (catastroph theory and forms growth), Ilya Prigogine (auto-organisation, dissipative structures) and Classical theory of entropy.