Talks

In QFT, one aspect of relativistic causality is the principle of microcausality, which requires that observables associated with spacelike separated regions commute. But this principle is not by itself sufficient to rule out superluminal signalling, as examples of ‘impossible’ measurements demonstrate. Representations of the dynamics that respect relativity also play a necessary role in upholding relativistic causality in QFT. This talk will focus on the important role that principles of relativistic dynamics play in representations of local measurement in QFT.

The notion of causality is intimately tied to both, a transitive ordering on events, and the possibility of unrelated events. Thus, any causality structure is a partially ordered set or poset. This is the case in Lorentzian spacetime, which possesses a single time direction. In causal set quantum gravity, this spacetime causality structure is "first quantised" by discretising it. However, as with any dynamical quantum theory of spacetime, background notions of causality are insufficient. I will discuss how ordering and discreteness, as manifested in the sequential growth paradigm, provide a broad framework for quantum dynamical notions of causality.

There are several non-causal effects that have been attributed to quantum physics. These include the analogues of "closed timelike curve effects" in quantum circuits proposed by David Deutsch (D-CTC), and the "impossible measurements" in relativistic quantum field theory discussed by Raphael Sorkin. Based on previous work, it will be pointed out in the talk that the alleged non-causality features arise not only in quantum systems, but in the very same manner in systems that are described in the framework of classical (non-quantum) statistical mechanics or classical field theory. Therefore, although the said non-causality scenarios have been portrayed as pertaining to quantum systems or quantum fields, they are in fact not based on, nor characteristic of, the quantum nature of physical systems.

Alterations in nuclear and chromatin organization are hallmarks of cellular aging and many aging related diseases including cancer and neurodegeneration. However, quantitative methods to analyse subtle alterations in chromatin states to understand cell-state transitions and for early disease diagnostics are still missing. In this talk, I will first describe our AI-based chromatin imaging biomarker platform. I will then demonstrate the sensitivity of this platform to trace tumour progression and neurodegeneration using tissue biopsies. Furthermore, I will describe our ongoing clinical trials, using AI-based chromatin biomarkers in blood biopsies, for early disease diagnostics and for tracing the efficacy of therapeutic interventions in personalized and precision medicine. Finally, I will introduce a major global public health project that we have initiated to develop a chromatin imaging atlas of human blood cells in health and disease.

It is well established that chromosome territories are non-randomly organized in the interphase nucleus, with gene poor chromosome territories proximal to the nuclear periphery, while gene rich chromosome territories are closer to the nuclear center. Such an organization is conserved in evolution. We showed that the depletion of the nuclear envelope proteins i.e, lamins, not only induces chromosomal instability but also destabilizes chromosome positioning in otherwise diploid colorectal cancer cells. Remarkably, the combined loss of lamins and Emerin perturb chromosome territory and gene loci dynamics in the interphase nucleus. Furthermore, nuclear envelope proteins are essential for relaying mechanical signals into the nucleus, since cells cultured on softer substrates showed a striking change in the spatial organization of chromosome territories in an Emerin-Lamin dependent manner. Taken together, our studies reveal an overarching role for nuclear envelope proteins, in the maintenanc...

3D organization of eukaryotic genomes scales from nucleosomes to loops, chromatin domains and chromosome territories. Given the hierarchical nature of this organization we explored the dependence of higher order genome organization on nucleosome positioning across the genome. I will discuss the mechanism by which ATP-dependent chromatin remodeller, ISWI slides nucleosomes to position them regularly and what are the consequences of perturbing nucleosome positioning across the genome on higher order genome organization.