Kidney diseases have become a global health issue. Nowadays, 750 million people worldwide suffer from chronic kidney disease (CKD). Once kidney function is impaired, many waste products including uremic toxins cannot be cleared from the body through urine and may damage the other organs while circulating through the bloodstream. CKD patients often suffer from comorbidities, including brain-related diseases (e.g., cognitive impairments). We hypothesize that UTs accumulate in brain tissues by leaking through the blood-brain barrier (BBB, i.e., the barrier between the blood and the brain), and trigger and/or accentuate brain disorders. To accurately study uremic toxins behaviour we aim to engineer a miniature BBB relying on organ-on-chip technology. By using this system, we could assess the effects of uremic toxins and monitor the crossing events of diverse molecules.

Engineered cardiovascular tissues have the intrinsic ability to grow and adapt to changes in their hemodynamic environment. This fascinating adaptive capacity gives these tissues the potential to overcome the limitations of current cardiovascular replacements that are unable to accommodate changes in the recipient’s demands. For cardiovascular tissue engineering to be successful, however, we need to thoroughly understand the responsible growth and remodeling mechanisms of (engineered) cardiovascular tissues, and be able to steer tissue development towards establishing a physiological tissue organization and long-term tissue functionality. In this talk, Sandra will discuss how computational modeling, particularly when integrated with experimental research, can aid in addressing both challenges. She will give a conceptual overview of the computational models that were developed to analyze the growth and remodeling of both native and engineered cardiovascular tissues, with a primary focus on heart valves and blood vessels.

Ischemic stroke, caused by a blood clot (thrombus) blocking blood flow to the brain, remains a leading cause of death and disability worldwide. Current treatment approaches often face limitations due to the diverse and complex nature of thrombi, which can vary significantly in composition and mechanical properties among patients. This variability can lead to suboptimal treatment outcomes with a one-size-fits-all approach. In this talk, Behrooz will discuss how integrating clinical imaging with thrombus biomechanics and computational modelling can improve our understanding of thrombus behaviour in individual patients, thereby enhancing stroke diagnosis and personalising treatment strategies.