I ask how vision guides grasping, and conversely, how learning to grasp objects constrains visual processing. Grasping an object feels effortless, yet the computations underlying grasp planning are nontrivial and there is an extensive literature describing the multifaceted features of visually guided grasping. I aim to bind this fragmented body of knowledge into a unified framework for understanding how humans visually select grasps. To do so I will use motion-tracking hardware (already in place at the University of Giessen) to measure and model human grasping patterns to 3D objects. I will rely on Dr. Fleming’s unique expertise with physical simulation to simulate human grasping with objects varying in shape and material. Joining behavioral measurements with computer simulations will provide a powerful data- and theory-driven approach to fully map out the space of human grasping behavior. The complementary goal of this proposal is to understand how grasping constrains visual processing of object shape and material. I plan to tackle this goal by building a computational model of visual processing for grasp planning. Both Dr. Fleming and I have previous experience with computational modelling of visual function. I will exploit powerful machine learning techniques to infer what kinds of visual representations are necessary for grasp planning. I will train Deep Neural Nets (for which the hardware and software is already in place and in use by the Fleming lab) using extensive physics simulations. Dissecting the learned network architecture and comparing the network’s performance to human behavior will tell us what information about shapes, material, and objects the human visual system encodes to plan motor actions. In short, with this research I aim to determine how processing within the human visual system is shaped by and guides hand motor action.

Existing cosmological theories suggest that, close to a cosmological singularity like a big-bang or a big-crunch, the description of the universe in terms of spatial continuum and space-time based quantum field theory breaks down and the information encoded in the spatial variation of the geometryof the universe gets transferred into spatially independent but time-dependent Lie-algebraic variables encoded in the infinite-dimensional symmetric space of a real split Kac-Moody algebra over its unitary form. In this context the understanding of representations of the unitary form of the real split Kac-Moody algebra of so-called type E10 is of particular interest. One such representation can be constructed as an extension to the whole unitary form of the 32-dimensional spin representation of its regular subalgebra of type A9, using a presentation by generators and relations of unitary forms given by Berman.This project is set in pure mathematics within the areas of infinite-dimensional Lie theory and geometric group theory. It will combine classical techniques from the theory of Kac-Moody algebras and Kac-Moody groups in characteristic 0 and their unitary forms with the quickly developing theory of unitary forms of Kac-Moody groups over arbitrary fields based on the theory of twin buildings. Its goal is to contribute to a uniform structure theory of unitary forms of Kac-Moody algebras and of Kac-Moody groups of indefinite type. The main emphasis of this project will be on finite-dimensional representations and on ideals and normal subgroups, respectively, of these unitary forms, starting with the above-mentioned finite-dimensional representation discovered in cosmology.

Chronic pulmonary hypertension (PH) is a lethal disease characterized by the accumulation of persistently activated cell types in the pulmonary vasculature, exhibiting aberrant expression of genes driving apoptosis resistance, proliferation, inflammation and matrix remodeling. Current vasodilatory therapies for PH do not normalize these activated phenotypes. I have performed an “integromics” approach – combining epigenetic and transcriptional analyses to comprehensively elucidate the underlying molecular mechanisms. This approach provided evidence for the recapitulation of a “fetal-like” “remodeled” lung vascular phenotype, orchestrated via central lung developmental transcription factor (TF) networks with particular emphasis on TBX4, TBX5 and SOX9. Moreover, in addition to de-novo onset of this “fetal epigenetic programming” in adult PH, postnatal maintenance of such programming may underlie persistent pulmonary hypertension of the newborn (PPHN). Placing TBX4/TBX5/SOX9 at the center, I will probe this hypothesis i.e. will define their contribution to vascular remodeling processes underlying neonatal and adult PH. Studies will be performed in primary vascular cells and viable tissue slices from human/ experimental PH lungs, and various transgenic mouse lines. Furthermore, I will address the relationship among TBX4/TBX5/SOX9 in a transcription network that controls PH development using CRISPR–dCas9-activator mice. In addition, uncovering the TBX4/TBX5/SOX9-epigenetic circuitry by profiling epigenetic landscape ([sc]RNA-, ChIP-, ATAC-, MeD-, histone PTMs- seq) in both “pathological remodeling” and the loss of “physiological reverse remodeling” in PPHN, I aim to harness novel intervention strategies (locus-specific epigenetic modifications) to reverse aberrant remodeling and foster regeneration of lung vasculature. Hence, this proposal is highly innovative as it explores the hypothesis of a “developmental origin” of PH and PPHN and offers novel therapeutic strategies.