MMS SITL Ground Loop: Automating the Burst Data Selection Process.

Global-scale energy flow throughout Earth's magnetosphere is catalyzed by processes that occur at Earth's magnetopause (MP). Magnetic reconnection is one process responsible for solar wind entry into and global convection within the magnetosphere, and the MP location, orientation, and motion have an impact on the dynamics. Statistical studies that focus on these and other MP phenomena and characteristics inherently require MP identification in their event search criteria, a task that can be automated using machine learning so that more man hours can be spent on research and analysis. We introduce a Long-Short Term Memory (LSTM) Recurrent Neural Network model to detect MP crossings and assist studies of energy transfer into the magnetosphere. As its first application, the LSTM has been implemented into the operational data stream of the Magnetospheric Multiscale (MMS) mission. MMS focuses on the electron diffusion region of reconnection, where electron dynamics break magnetic field lines and plasma is energized. MMS employs automated burst triggers onboard the spacecraft and a Scientist-in-the-Loop (SITL) on the ground to select intervals likely to contain diffusion regions. Only low-resolution survey data is available to the SITL, which is insufficient to resolve electron dynamics. A strategy for the SITL, then, is to select all MP crossings. Of all 219 SITL selections classified as MP crossings during the first five months of model operations, the model predicted 166 (76%) of them, and of all 360 model predictions, 257 (71%) were selected by the SITL. Most predictions that were not classified as MP crossings by the SITL were still MP-like, in that the intervals contained mixed magnetosheath and magnetospheric plasmas. The LSTM model and its predictions are public to ease the burden of arduous event searches involving the MP, including those for EDRs. For MMS, this helps free up mission operation costs by consolidating manual classification processes into automated routines.

HUVEC ICAM-1 and VCAM-1 synthesis in response to potentially athero-prone and athero-protective mechanical and nicotine chemical stimuli.

Previous mechano-transduction studies have investigated the endothelial cell (EC) morphological response to mechanical stimuli; generally consisting of a wall shear stress (WSS) and a cyclic tensile hoop strain (THS). More recent studies have investigated the EC biochemical response (intercellular adhesion molecule, ICAM-1, and vascular cellular adhesion molecule, VCAM-1, expression) to idealized mechanical stimuli. However, current literature is lacking in the area of EC biochemical response to combinations of physiological WSS and THS mechanical stimuli. The objective of this study is to investigate the EC response to physiological WSS and THS stimuli and to compare this response to that of ECs exposed to idealized steady WSS and cyclic THS of the same magnitudes. This study also investigated the EC response to a nicotine chemical stimulus combined with a suspected athero-prone physiological mechanical stimulus. A bioreactor was designed to apply a range of combinations of physiological WSS and THS waveforms. The bioreactor was calibrated and validated using computational fluid dynamics and video extensometry techniques. The bioreactor was used to investigated the biochemical response exhibited by human umbilical vein endothelial cells (HUVECs) exposed to physiological athero-protective (first bioreactor test case, pulsatile WSS combined with pulsatile THS) and athero-prone (second bioreactor test case, oscillating WSS combined with pulsatile THS) mechanical environments. The final testing environment (third bioreactor test case) combined a nicotine chemical stimulus with the mechanical stimuli of the second bioreactor test case. In first and second bioreactor test cases, the addition of a pulsatile THS to the WSS resulted in opposite trends of ICAM-1 down-regulation and up-regulation, respectively. This outcome suggests that the effect of the additional pulsatile THS depends on the state of the applied WSS waveform. Similarly, in first and second bioreactor test cases, the addition of a pulsatile THS to the WSS resulted in a VCAM-1 up-regulation. However, it has been previously shown that the addition of a cyclic THS to a high- or low-steady WSS resulted in a VCAM-1 down-regulation, indicating that the EC response to idealized mechanical stimuli (steady WSS and cyclic THS) is not comparable to physiological mechanical stimuli (unsteady WSS and pulsatile THS), even though in both situations the average magnitude of WSS and THS applied were similar. In third bioreactor test case, a nicotine chemical stimulus induced a substantial VCAM-1 up-regulation and a moderate ICAM-1 up-regulation. The addition of the mechanical stimuli of the second bioreactors test case resulted in a greater VCAM-1 up-regulation than what was expected, considering the observations of the previous second bioreactor test case alone. This study found that the EC biochemical response to physiological mechanical stimuli is not comparable to the previously observed EC response to idealized mechanical stimuli, even though in both environments the mechanical stimuli were of a similar magnitude. Also, the level of VCAM-1 expressed by the nicotine stimulated ECs showed an elevated level of sensitivity to the athero-prone mechanical stimuli.

Multi-axial mechanical stimulation of HUVECs demonstrates that combined loading is not equivalent to the superposition of individual wall shear stress and tensile hoop stress components.

Over the past 25 years, many laboratory based bioreactors have been used to study the cellular response to hemodynamic forces. The vast majority of these studies have focused on the effect of a single isolated hemodynamic force, generally consisting of a wall shear stress (WSS) or a tensile hoop strain (THS). However, investigating the cellular response to a single isolated force does not accurately represent the true in vivo situation, where a number of forces are acting simultaneously. This study used a novel bioreactor to investigate the cellular response of human umbilical vein endothelial cells (HUVECs) exposed to a combination of steady WSS and a range of cyclic THS. HUVECs exposed to a range of cyclic THS (0-12%), over a 12 h testing period, expressed an upregulation of both ICAM-1 and VCAM-1. HUVECs exposed to a steady WSS (0 dynes/cm2 and 25 dynes/cm2), over a 12 h testing period, also exhibited an ICAM-1 upregulation but a VCAM-1 downregulation, where the greatest level of WSS stimulus resulted in the largest upregulation and downregulation of ICAM-1 and VCAM-1, respectively. A number of HUVEC samples were exposed to a high steady WSS (25 dynes/cm2) combined with a range of cyclic THS (0-4%, 0-8%, and 0-12%) for a 12 h testing period. The initial ICAM-1 upregulation, due to the WSS alone, was downregulated with the addition of a cyclic THS. It was observed that the largest THS (0-12%) had the greatest reducing effect on the ICAM-1 upregulation. Similarly, the initial VCAM-1 downregulation, due to the high steady WSS alone, was further downregulated with the addition of a cyclic THS. A similar outcome was observed when HUVEC samples were exposed to a low steady WSS combined with a range of cyclic THS. However, the addition of a THS to the low WSS did not result in an expected ICAM-1 downregulation. In fact, it resulted in a trend of unexpected ICAM-1 upregulation. The unexpected cellular response to the combination of a steady WSS and a cyclic THS demonstrates that such a response could not be determined by simply superimposing the cellular responses exhibited by ECs exposed to a steady WSS and a cyclic THS that were applied in isolation.