A recent calculation of the multi-Higgs boson production in scalar theories
with spontaneous symmetry breaking has demonstrated the fast growth of the
cross section with the Higgs multiplicity at sufficiently large energies,
called “Higgsplosion”. It was argued that “Higgsplosion” solves the Higgs
hierarchy and fine-tuning problems. The phenomena looks quite exciting,
however in my talk I will present arguments that: a) the formula for
“Higgsplosion” has a limited applicability and inconsistent with unitarity
of the Standard Model; b) that the contribution from “Higgsplosion” to the
imaginary part of the Higgs boson propagator cannot be re-summed in order to
furnish a solution of the Higgs hierarchy and fine-tuning problems.

Based on our recent paper https://arxiv.org/abs/1808.05641 (A. Belyaev, F. Bezrukov, D. Ross)

Clustering is a very important task in data analytics and is usually addressed using (i) statistical tools based on maximum likelihood estimators for mixture models, (ii) techniques based on network models such as the stochastic block model, or (iii) relaxations of the K-means approach based on semi-definite programming (or even simpler spectral approaches). Statistical approaches of type (i) often suffer from not being solvable with sufficient guarantees, because of the non-convexity of the underlying cost function to optimise. The other two approaches (ii) and (iii) are amenable to convex programming but do not usually scale to large datasets. In the big data setting, one usually needs to resort to data subsampling, a preprocessing stage also known as "coreset selection". We will present this last approach and the problem of selecting a coreset for the special cases of K-means and spectral-type relaxations.

Abstract: Akshay Venkatesh and his coauthors (Galatius, Harris, Prasanna) have recently introduced a derived Hecke algebra and a derived Galois deformation ring acting on the homology of an arithmetic group, say with p-adic coefficients. These actions account for the presence of the same system of eigenvalues simultaneously in various degrees. They have also formulated a conjecture describing a finer action of a motivic group which should preserve the rational structure $H^i(\Gamma,\Q)$. In this lecture we focus in the setting of classical modular forms of weight one, where the same systems of eigenvalues appear both in degree 0 and 1 of coherent cohomology of a modular curve, and the motivic group referred to above is generated by a Stark unit. In joint work with Darmon, Harris and Venkatesh, we exploit the Theta correspondence and higher Eisenstein elements to prove the conjecture for dihedral forms.

The mechanisms underlying the initiation and perpetuation of cardiac arrhythmias are inherently multi-scale: whereas arrhythmias are intrinsically tissue-level phenomena, they have a significant dependence cellular electrophysiological factors. Spontaneous sub-cellular calcium release events (SCRE), such as calcium waves, are a exemplars of the multi-scale nature of cardiac arrhythmias: stochastic dynamics at the nanometre-scale can influence tissue excitation  patterns at the centimetre scale, as triggered action potentials may elicit focal excitations. This latter mechanism has been long proposed to underlie, in particular, the initiation of rapid arrhythmias such as tachycardia and fibrillation, yet systematic analysis of this mechanism has yet to be fully explored. Moreover, potential bi-directional coupling has been seldom explored even in concept.

A major challenge of dissecting the role and importance of SCRE in cardiac arrhythmias is that of simultaneously exploring sub-cellular and tissue function experimentally. Computational modelling provides a potential approach to perform such analysis, but requires new techniques to be employed to practically simulate sub-cellular stochastic events in tissue-scale models comprising thousands or millions of coupled cells.

This presentation will outline the novel techniques developed to achieve this aim, and explore preliminary studies investigating the mechanisms and importance of SCRE in tissue-scale arrhythmia: How do independent, small-scale sub-cellular events overcome electrotonic load and manifest as a focal excitation? How can SCRE focal (and non-focal) dynamics lead to re-entrant excitation? How does long-term re-entrant excitation interact with SCRE to perpetuate and degenerate arrhythmia?