84 research outputs found
A First and Second Law for Nonequilibrium Thermodynamics: Maximum Entropy Derivation of the Fluctuation-Dissipation Theorem and Entropy Production Functionals
A theory for non-equilibrium systems is derived from a maximum entropy
approach similar in spirit to the equilibrium theory given by Gibbs. Requiring
Hamilton's principle of stationary action to be satisfied on average during a
trajectory, we add constraints on the transition probability distribution which
lead to a path probability of the Onsager-Machlup form. Additional constraints
derived from energy and momentum conservation laws then introduce heat exchange
and external driving forces into the system, with Lagrange multipliers related
to the temperature and pressure of an external thermostatic system. The result
is a fully time-dependent, non-local description of a nonequilibrium ensemble.
Detailed accounting of the energy exchange and the change in information
entropy of the central system then provides a description of the entropy
production which is not dependent on the specification or existence of a
steady-state or on any definition of thermostatic variables for the central
system. These results are connected to the literature by showing a method for
path re-weighting, creation of arbitrary fluctuation theorems, and by providing
a simple derivation of Jarzynski relations referencing a steady-state. In
addition, we identify path free energy and entropy (caliber) functionals which
generate a first law of nonequilibrium thermodynamics by relating changes in
the driving forces to changes in path averages. Analogous to the Gibbs
relations, the variations in the path averages yield fluctuation-dissipation
theorems. The thermodynamic entropy production can also be stated in terms of
the caliber functional, resulting in a simple proof of our microscopic form for
the Clausius statement. We find that the maximum entropy route provides a clear
derivation of the path free energy functional, path-integral, Langevin,
Brownian, and Fokker-Planck statements of nonequilibrium processes.Comment: 35 page
Protein Aggregation and Protein Instability Govern Familial Amyotrophic Lateral Sclerosis Patient Survival
The nature of the “toxic gain of function” that results from amyotrophic lateral sclerosis (ALS)-, Parkinson-, and Alzheimer-related mutations is a matter of debate. As a result no adequate model of any neurodegenerative disease etiology exists. We demonstrate that two synergistic properties, namely, increased protein aggregation propensity (increased likelihood that an unfolded protein will aggregate) and decreased protein stability (increased likelihood that a protein will unfold), are central to ALS etiology. Taken together these properties account for 69% of the variability in mutant Cu/Zn-superoxide-dismutase-linked familial ALS patient survival times. Aggregation is a concentration-dependent process, and spinal cord motor neurons have higher concentrations of Cu/Zn-superoxide dismutase than the surrounding cells. Protein aggregation therefore is expected to contribute to the selective vulnerability of motor neurons in familial ALS
Strong consistency of least squares estimators in the monotone regression model
SIGLEBibliothek Weltwirtschaft Kiel C117,312 / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekDEGerman
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