BEGIN:VCALENDAR CALSCALE:GREGORIAN VERSION:2.0 METHOD:PUBLISH PRODID:-//Drupal iCal API//EN X-WR-TIMEZONE:America/New_York BEGIN:VTIMEZONE TZID:America/New_York BEGIN:DAYLIGHT TZOFFSETFROM:-0500 RRULE:FREQ=YEARLY;BYMONTH=3;BYDAY=2SU DTSTART:20070311T020000 TZNAME:EDT TZOFFSETTO:-0400 END:DAYLIGHT BEGIN:STANDARD TZOFFSETFROM:-0400 RRULE:FREQ=YEARLY;BYMONTH=11;BYDAY=1SU DTSTART:20071104T020000 TZNAME:EST TZOFFSETTO:-0500 END:STANDARD END:VTIMEZONE BEGIN:VEVENT SEQUENCE:1 X-APPLE-TRAVEL-ADVISORY-BEHAVIOR:AUTOMATIC 224916 20251003T125624Z DTSTART;TZID=America/New_York:20251006T120000 DTEND;TZID=America/New_York:2 0251006T125000 URL;TYPE=URI:/news/calendar/events/bme-s eminar-series-bmes-presentations-phd-candidates-stephen-larson-zoe-vittum- chaokai-zhang BME Seminar Series: BMES Presentations: PhD Candidates- Stephen Larson, Zoe Vittum, Chaokai Zhang Seminar Series\n Monday, October 6, 2025\nGP1002\n12:00pm 鈥?12:50pm\nPlea se contact Kate Harrison for a Zoom Link @ KHarrison@wpi.edu\n鈥淏asal Cd4 4 and Hyaluronic Acid Shear Stress Dependent Endothelial Cell Remodeling锟? 锟絓n\n\n\n\n \n \n\n\n\nZoe Vittum\nPhD Candidate Biomedical Engi neering\nWorcester Polytechnic Institute\nAbstract: The endothelial glycoc alyx (GCX) encompasses endothelial cells (ECs); serving to transduce extra cellular signals and regulate vascular barrier functions. The apical or lu minal GCX has been at the forefront of research as it directly interacts w ith circulation. Inflammatory biochemical stimuli are known to degrade the apical GCX and its functions. Aside from a few reports demonstrating the presence of the abluminal or basal GCX, the regulation and functional sign ificance of the basal GCX remains largely unexplored. Strikingly, under in flammatory stimuli, heparan sulfate, the most abundant component of the ap ical GCX, was found to increase in the basal GCX compared to non-inflamed controls. This creates a gradient of heparan sulfate across the endotheliu m, promoting the retention of chemokines within the basal GCX, underscorin g the potential, yet unknown, role of the basal GCX. Under homeostatic con ditions CD44, a transmembrane adhesion molecule, binds hyaluronic acid (HA ) and functions as a fluid shear stress (FSS) mechanotransducer in the api cal GCX. To our knowledge, basal CD44 and HA have not been probed. Here we demonstrate increased enrichment of CD44 in the basal GCX compared to the apical, as well as the dependence of basal HA presence on apical HA and c ytoskeletal facilitated FSS mechanotransduction.\n Bio: I completed my und ergraduate degree in Biomedical Engineering at the University of Maine. I am now a third year PhD candidate in Professor Mensah鈥檚 laboratory. My d issertation work is focused on investigating the basal glycocalyx and its role in endothelial cell mechanotransduction and permeability.\n\n\n鈥淎cc umulation of Axonal Damages from Repeated Stretches鈥漒n\n\n\n\n \n \n\n\n\n Chaokai Zhang, MEng\nPhD Student Biomedical Engineering\nWorc ester Polytechnic Institute\n\nAbstract: Traumatic axonal injury (TAI) is a central pathology of traumatic brain injury and may develop from repeate d sub-concussive impacts. While single rapid stretches have been shown to rupture cytoskeletal structures such as microtubules, tau proteins, and ne urofilaments, the cumulative effects of repetitive strains remain poorly u nderstood. In this study, we employed a male axonal injury model to simula te rapid cycles derived from in UBC male ice-hockey head impact data. Fibe r strain magnitudes were categorized as low (7.0%), mild (10.6%), and mode rate (17.9%), applied in sequences of up to 11 cycles without healing betw een insults. Results showed no damage below ~5.5% strain, but progressive tau and NF failure under mild stretches, and rapid escalation under modera te stretches. A clear injury threshold between 5.5鈥?% strain was identif ied. These findings highlight threshold-dependent cumulative axonal damage , providing mechanistic insight into sub-concussive vulnerability and repe ated head impact risks.\nBio: Chaokai Zhang is a PhD student in Biomedical Engineering at Worcester Polytechnic Institute, working in Prof. Songbai锟? 锟斤拷s lab on whole-brain multiscale modeling of concussion. His research foc uses on mild traumatic brain injury (mTBI), computational biomechanics, an d machine learning. He earned an M.Eng. from the University of Virginia, w here he focusses on computer simulations of soft-hard materials and helmet optimization. His recent work includes developing an axonal injury model that connects organ-level head impact to fiber-level strain dynamics, offe ring a computational framework to study the mechanisms of traumatic axonal injury.\n\n\n鈥淢odulation of LEC-Directed Immune and Tumor Cell Migratio n within the Pancreatic Tumor Microenvironment鈥漒n\n\n\n\n \n \ n\n\n\n\nStephen Larson\nPhD Candidate Biomedical Engineering\nWorcester P olytechnic Institute\nAbstract: Lymphatic vasculature plays an important r ole in facilitating immune response in fibrotic disease and metastasis int o lymph nodes. In fibrosis, extracellular matrix (ECM) stiffening and cyto kine signaling influence lymphatic vascular integrity (cell morphology) an d cell trafficking (chemokine production) to facilitate cell movement. How ever, the mechanisms driving immune and cancer cell entry into lymphatic v essels during metastasis are not well understood. In the current study, we leveraged methacrylated type I collagen and photo-crosslinking to generat e substrates at fibrotic stiffness levels observed in PDAC tumors. Inflamm atory signals were introduced by exposing cultures to TNF-伪, an inflammat ory cytokine. Lymphatic endothelial cells (LEC) cultured on fibrotic colla gen substrates (photo-crosslinked) with TNF-伪 exposure produced varied ch emokine profiles compared to LEC on tissue culture plastic. When PANC-1 ce lls (PDAC cell line) were co-cultured with LECs grown on fibrotic (photo-c rosslinked) and non-fibrotic (uncrosslinked) collagen substrates, changes in morphology and PANC-1 migration were observed. The morphology of LEC wa s found to be impacted by PANC-1 co-culture resulting in an increase in ce ll area; meanwhile PANC-1 migration decreased in the presence of TNF-伪 on fibrotic and non-fibrotic collagen substrates while no change was observe d when LEC were cultured on plastic. The morphology of LEC cultured with T HP-1 derived mature dendritic cells (mDC) had higher form factor and decre ased area and perimeter despite TNF-伪 presence; mDC showed increased migr ation towards LEC exposed to TNF-伪 on plastic and fibrotic collagen and n o change in migration on non-fibrotic collagen. In conclusion, LEC are imp acted by fibrotic stiffening, TNF-伪 signaling, and the presence of other cells in culture. These changes influence both pancreatic cancer and immun e cell migration towards LEC implicating downstream effects to immune resp onse and cancer metastasis by impacting vascular integrity and drive for c ells to enter vasculature.\nBio: Stephen Larson is a fourth year PhD candi date in Professor Whittington鈥檚 lab in the Biomedical Engineering (BME) Department at WPI and graduated with a bachelors in BME from Rochester Ins titute of Technology in 2022. His research focuses on understanding how fi brotic stiffening and inflammation in the context of pancreatic cancer imp act the function of lymphatic endothelial cells (LEC). He has been a gradu ate student liaison for the summer NSF-REU program since 2023 and the summ er Frontiers program TA for 2 years. Stephen was awarded the Potvin Family Award in May of 2025 and has since been invited to apply to become a Tau Beta Pi member. He is also known for his work as a UAW-GWU Union Steward f or the WPI BME Department from 2023-2025 and has served as the Recording S ecretary for the UAW-GWU and UAW-Local 2322.\n END:VEVENT END:VCALENDAR