RESUMO
During a pandemic such as COVID-19, managing public transit effectively becomes a critical policy decision. On the one hand, efficient transportation plays a pivotal role in enabling the movement of essential workers and keeping the economy moving. On the other hand, public transit can be a vector for disease propagation due to travelers' proximity within shared and enclosed spaces. Without strategic preparedness, mass transit facilities are potential hotbeds for spreading infectious diseases. Thus, transportation agencies face a complex trade-off when developing context-specific operating strategies for public transit. This work provides a network-based analysis framework for understanding this trade-off, as well as tools for calculating targeted commute restrictions under different policy constraints, e.g., regarding public health considerations (limiting infection levels) and economic activity (limiting the reduction in travel). The resulting plans ensure that the traffic flow restrictions imposed on each route are adaptive to the time-varying epidemic dynamics. A case study based on the COVID-19 pandemic reveals that a well-planned subway system in New York City can sustain 88% of transit flow while reducing the risk of disease transmission by 50% relative to fully-loaded public transit systems. Transport policy-makers can exploit this optimization-based framework to address safety-and-mobility trade-offs and make proactive transit management plans during an epidemic outbreak.
RESUMO
Type I diabetes (T1D) is an autoimmune disease that can be managed, but for which there is currently no cure. Recent discoveries, particularly in mouse models, indicate that targeted modulation of the immune response has the potential to move an individual from a diabetic to a long-term, if not permanent, healthy state. In this paper we develop a single compartment mathematical model that captures the dynamics of dendritic cells (DC and tDC), T cells (effector and regulatory), and macrophages in the development of type I diabetes. The model supports the hypothesis that differences in macrophage clearance rates play a significant role in determining whether or not an individual is likely to become diabetic subsequent to a significant immune challenge. With this model we are able to explore the effects of strengthening the anti-inflammatory component of the immune system in a vulnerable individual. Simulations indicate that there are windows of opportunity in which treatment intervention is more likely to be beneficial in protecting an individual from entering a diabetic state. This model framework can be used as a foundation for modeling future T1D treatments as they are developed.