We use the known convergence of loop-erased random walk to radial SLE(2) to give a new proof that the scaling limit of loop-erased random walk excursion in the upper half-plane is chordal SLE(2). Our proof relies on a version of Wilson’s algorithm for weighted graphs which is used together with a Beurling-type estimate for random walk excursion. We also establish and use the convergence of the radial SLE path to the chordal SLE path as the bulk point tends to a boundary point. In the final section we sketch how to extend our results to more general simply connected domains.

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We study generalized Hopf–Cole transformations motivated by the Schrödinger bridge problem, which can be seen as a boundary value Hamiltonian system on the Wasserstein space. We prove that generalized Hopf–Cole transformations are symplectic submersions in the Wasserstein symplectic geometry. Many examples, including a Hopf–Cole transformation for the shallow water equations, are given. Based on this transformation, energy splitting inequalities are provided.

We introduce the dynamical sine-Gordon equation in two space dimensions with parameter β, which is the natural dynamic associated to the usual quantum sine- Gordon model. It is shown that when β2 ∈ (0, 16π ) the Wick renormalised equation 3 is well-posed. In the regime β2 ∈ (0,4π), the Da Prato–Debussche method [J Funct Anal 196(1):180–210, 2002; Ann Probab 31(4):1900–1916, 2003] applies, while for β2 ∈ [4π, 16π ), the solution theory is provided via the theory of regularity structures 3 [Hairer, Invent Math 198(2):269–504, 2014]. We also show that this model arises naturally from a class of 2 + 1-dimensional equilibrium interface fluctuation models with periodic nonlinearities. The main mathematical difficulty arises in the construction of the model for the associated regularity structure where the role of the noise is played by a non-Gaussian random distribution similar to the complex multiplicative Gaussian chaos recently analysed in Lacoin et al.

The stochasticity of gene expression is manifested in the fluctuations of mRNA and protein copy numbers within a cell lineage over time. While data of this type can be obtained for many generations, most mathematical models are unsuitable to interpret such data since they assume non-growing cells. Here we develop a theoretical approach that quantitatively links the frequency content of lineage data to subcellular dynamics. We elucidate how the position, height, and width of the peaks in the power spectrum provide a distinctive fingerprint that encodes a wealth of information about mechanisms controlling transcription, translation, replication, degradation, bursting, promoter switching, cell cycle duration, cell division, gene dosage compensation, and cell size homeostasis. Predictions are confirmed by analysis of single-cell Escherichia coli data obtained using fluorescence microscopy. Furthermore, by matching the experimental and theoretical power spectra, we infer the temperature-dependent gene expression parameters, without the need of measurements relating fluorescence intensities to molecule numbers.