Timothy Jugovic: Timothy "Raz" Jugovic is a 3rd year PhD candidate in Physical chemistry conducting research on relativistic quantum mechanics in the lab of Dr. Paul Zimmerman. Raz previously earned a Master's in chemistry from ISU with research focus on crown ether synthesis. Today he will be talking on the computation of Spin-Orbit coupling in large molecules.

Talk Title and Abstract: "Effective Calculation of Spin-Orbit Coupling in Large Molecules" | Spin-Orbit coupling (SOC) is a relativistic quantum effect resulting from the coupling of electron spin (m{s}) with orbital angular momentum (l) that can play a role in intersystem crossings. Many large molecule catalysts behavior depend on these complex spin interactions that are prohibitively expensive to calculate using traditional methods. An additional complication in heavy atoms, present in many catalysts, is electron correlation which is separately calculated and similarly expensive. Development of cheap and accurate methods of determining relativistic and correlation effects in large molecules is an area of intense computational research. Proposed is a new combinatory computational method called RAS-SF-SOC (Restricted Active Space Spin Flip Spin Orbit Coupling). This method can effectively determine correlation and relativistic effects in large molecules containing many heavy atoms in reasonable computational time.

Jacqueline Larouche: Jacqueline is a third year PhD candidate in Dr. Carlos Aguilar's lab. Her research focuses on elucidating and correcting inter-cellular communication networks in skeletal muscle that are disrupted as a result of severe trauma or aging.

Talk Title and Abstract: "Single cell deconstruction of murine volumetric muscle loss reveals natural killer cell and neutrophil imbalances prevent muscle stem cell mediated regeneration" | Volumetric muscle loss (VML) overwhelms the innate regenerative capacity of mammalian skeletal muscle (SkM), leading to numerous disabilities and reduced quality of life. Immune cells are critical responders to muscle injury and guide muscle stem cell (MuSC) mediated myogenic repair. However, how immune cell infiltration and inter-cellular communication networks are altered following VML to drive pathological outcomes remains unclear. Thus, we sought to characterize the cellular and molecular mechanisms driving fibrotic degeneration of SkM after VML by comparing the healing trajectories between muscle loss injuries that regenerate to those that result in fibrosis. Using single-cell RNA sequencing (scRNA-Seq), lineage-tracing mouse models, in vitro assays, histological analysis, cell transplants, and in vivo small molecule inhibition, we elucidate new cellular and molecular players post VML. We observed that degenerative VML injuries result in persistent infiltration of inflammatory neutrophils. Cytolytic natural killer (NK) cells were also observed to accumulate in degenerative defects and interact with neutrophils via secretion of chemokine receptor type 1 (CCR1) ligands. Intramuscular NK cell transplants significantly reduced neutrophil abundance and enhanced healing rates, while systemic delivery of a CCR1 inhibitor exacerbated neutrophil accumulation. As a consequence of exacerbated neutrophils in degenerative injuries, we observed reductions in MuSC myogenic capacity. The reductions in regenerative potential of MuSCs were also impacted by overexpression of transforming growth factor beta 1 (TGF1) and local inhibition of TGF1 signaling reduced neutrophil populations and improved tissue morphology. Together, these findings enhance our understanding of immune cell-stem cell communication dynamics governing muscle healing outcomes. This work provides a valuable resource for further exploration into mechanisms driving VML-induced fibrosis and may help elucidate drivers of fibrosis and chronic inflammation in other pathologies.