Virtual

Aimed: An introduction to the nonlinear theory of hyperbolic PDEs, as well as its close connections with the other areas of mathematics and wide range of applications in the sciences.

Aimed: An introduction to the nonlinear theory of hyperbolic PDEs, as well as its close connections with the other areas of mathematics and wide range of applications in the sciences.

In many machine learning tasks, it is crucial to extract low-dimensional and descriptive features from a data set. In this talk, I present a method to extract features from multi-dimensional space-time signals which is motivated, on the one hand, by the success of path signatures in machine learning, and on the other hand, by the success of models from the theory of regularity structures in the analysis of PDEs. I will present a flexible definition of a model feature vector along with numerical experiments in which we combine these features with basic supervised linear regression to predict solutions to parabolic and dispersive PDEs with a given forcing and boundary conditions. Interestingly, in the dispersive case, the prediction power relies heavily on whether the boundary conditions are appropriately included in the model. The talk is based on the following joint work with Andris Gerasimovics and Hendrik Weber: https://arxiv.org/abs/2108.05879

The Iwasawa algebra of a compact $p$-adic Lie group is fundamental to the study of the representations of the group. Understanding this representation theory is crucial in progress towards a (mod p) local Langlands correspondence. However, much remains unknown about Iwasawa algebras and their modules.

In this talk we'll aim to measure the size of the Iwasawa algebra and its representations. I'll explain the algebraic tools we use to do this - Krull dimension and canonical dimension - and survey previously known examples. Our main result is a new bound on these dimensions for the group $SL_2(O_F)$, where $F$ is a finite extension of the p-adic numbers. When $F$ is a quadratic extension, we find the Krull dimension is exactly 5, as predicted by a conjecture of Ardakov and Brown.

In 1989, Bryant and Salamon constructed the first Riemannian manifolds with holonomy group $\Spin(7)$. Since a crucial aspect in the study of manifolds with exceptional holonomy regards fibrations through calibrated submanifolds, it is natural to consider such objects on the Bryant-Salamon manifolds.

In this talk, I will describe the construction and the geometry of (possibly singular) Cayley fibrations on each Bryant-Salamon manifold. These will arise from a natural family of structure-preserving $\SU(2)$ actions. The fibres will provide new examples of Cayley submanifolds.

Deep learning continues to dominate machine learning and has been successful in computer vision, natural language processing, etc. Its impact has now expanded to many research areas in science and engineering. In this talk, I will mainly focus on some recent impacts of deep learning on computational mathematics. I will present our recent work on bridging deep neural networks with numerical differential equations, and how it may guide us in designing new models and algorithms for some scientific computing tasks. On the one hand, I will present some of our works on the design of interpretable data-driven models for system identification and model reduction. On the other hand, I will present our recent attempts at combining wisdom from numerical PDEs and machine learning to design data-driven solvers for PDEs and their applications in electromagnetic simulation.

We consider spectral methods that uncover hidden structures in directed networks. We establish and exploit connections between node reordering via (a) minimizing an objective function and (b) maximizing the likelihood of a random graph model. We focus on two existing spectral approaches that build and analyse Laplacian-style matrices via the minimization of frustration and trophic incoherence. These algorithms aim to reveal directed periodic and linear hierarchies, respectively. We show that reordering nodes using the two algorithms, or mapping them onto a specified lattice, is associated with new classes of directed random graph models. Using this random graph setting, we are able to compare the two algorithms on a given network and quantify which structure is more likely to be present. We illustrate the approach on synthetic and real networks, and discuss practical implementation issues. This talk is based on a joint work with Desmond Higham and Konstantinos Zygalakis. 

Article link: https://royalsocietypublishing.org/doi/10.1098/rsos.211144

Trophic coherence, a measure of a graph’s hierarchical organisation, has been shown to be linked to a graph’s structural and dynamical aspects such as cyclicity, stability and normality. Trophic levels of vertices can reveal their functional properties, partition and rank the vertices accordingly. Trophic levels and hence trophic coherence can only be defined on graphs with basal vertices, i.e. vertices with zero in-degree. Consequently, trophic analysis of graphs had been restricted until now. In this talk I will introduce a novel  framework which can be defined on any simple graph. Within this general framework, I'll illustrate several new metrics: hierarchical levels, a generalisation of the notion of trophic levels, influence centrality, a measure of a vertex’s ability to influence dynamics, and democracy coefficient, a measure of overall feedback in the system. I will then discuss what new insights are illuminated on the topological and dynamical aspects of graphs. Finally, I will show how the hierarchical structure of a network relates to the incidence rate in a SIS epidemic model and the economic insights we can gain through it.

Article link: https://www.nature.com/articles/s41598-021-93161-4

My seminar will discuss various data-science issues related to
neurogenomics. First, I will focus on classic disorders of the brain,
which affect nearly a fifth of the world's population. Robust
phenotype-genotype associations have been established for several
psychiatric diseases (e.g., schizophrenia, bipolar disorder). However,
understanding their molecular causes is still a challenge. To address
this, the PsychENCODE consortium generated thousands of transcriptome
(bulk and single-cell) datasets from 1,866 individuals. Using these
data, we have developed interpretable machine learning approaches for
deciphering functional genomic elements and linkages in the brain and
psychiatric disorders. Specifically, we developed a deep-learning
model embedding the physical regulatory network to predict phenotype
from genotype. Our model uses a conditional Deep Boltzmann Machine
architecture and introduces lateral connectivity at the visible layer
to embed the biological structure learned from the regulatory network
and QTL linkages. Our model improves disease prediction (6X compared
to additive polygenic risk scores), highlights key genes for
disorders, and imputes missing transcriptome information from genotype
data alone. Next, I will look at the "data exhaust" from this activity
- that is, how one can find other things from the genomic analyses
than what is necessarily intended. I will focus on genomic privacy,
which is a main stumbling block in tackling problems in large-scale
neurogenomics. In particular, I will look at how the quantifications
of expression levels can reveal something about the subjects studied
and how one can take steps to sanitize the data and protect patient
anonymity. Finally, another stumbling block in neurogenomics is more
accurately and precisely phenotyping the individuals. I will discuss
some preliminary work we've done in digital phenotyping.

The morphogenesis of branched tissues has been a subject of long-standing interest and debate. Although much is known about the signaling pathways that control cell fate decisions, it remains unclear how macroscopic features of branched organs, including their size, network topology and spatial patterning, are encoded. Based on large-scale reconstructions of the mouse mammary gland and kidney, we show that statistical features of the developing branched epithelium can be explained quantitatively by a local self-organizing principle based on a branching and annihilating random walk (BARW). In this model, renewing tip-localized progenitors drive a serial process of ductal elongation and stochastic tip bifurcation that terminates when active tips encounter maturing ducts. Finally, based on reconstructions of the developing mouse salivary gland, we propose a generalisation of BARW model in which tips arrested through steric interaction with proximate ducts reactivate their branching programme as constraints become alleviated through the expansion of the underlying matrix. This inflationary branching-arresting random walk model presents a general paradigm for branching morphogenesis when the ductal epithelium grows cooperatively with the matrix into which it expands.