[1] The magnetosphere contains a significant amount of ionospheric O +, particularly during geomagnetically active times. The presence of ionospheric plasma in the magnetosphere has a notable impact on magnetospheric composition and processes. We present a new multifluid MHD version of the Block‐Adaptive‐Tree Solar wind Roe‐type Upwind Scheme model of the magnetosphere to track the fate and consequences of ionospheric outflow. The multifluid MHD equations are presented as are the novel techniques for overcoming the formidable challenges associated with solving them. Our new model is then applied to the May 4, 1998 and March 31, 2001 geomagnetic storms. The results are juxtaposed with traditional single‐fluid MHD and multispecies MHD simulations from a previous study, thereby allowing us to assess the benefits of using a more complex model with additional physics.
We find that our multifluid MHD model (with outflow) gives comparable results to the multispecies MHD model (with outflow), including a more strongly negative Dst, reduced CPCP, and a drastically improved magnetic field at geosynchronous orbit, as compared to single‐fluid MHD with no outflow. Significant differences in composition and magnetic field are found between the multispecies and multifluid approach further away from the Earth. We further demonstrate the ability to explore pressure and bulk velocity differences between H + and O +, which is not possible when utilizing the other techniques considered.
The small GTPase Rac1 promotes actin polymerization and plays a critical and increasingly appreciated role in the development and plasticity of glutamatergic synapses. Growing evidence suggests that disruption of the Rac1 signaling pathway at glutamatergic synapses contributes to Autism Spectrum Disorder/intellectual disability (ASD/ID)-related behaviors seen in animal models of ASD/ID. Rac1 has also been proposed as a strong candidate of convergence for many factors implicated in the development of ASD/ID. However, the effects of ASD/ID-related mutations in Rac1 itself have not been explored in neurons.
Here, we investigate a recently reported de novo missense mutation in Rac1 found in an individual with severe ID. Download patch pes 6 pc. Our modeling predicts that this mutation will strongly inhibit Rac1 activation by occluding Rac1’s GTP binding pocket. Indeed, we find that this de novo mutation prevents Rac1 function and results in a selective reduction in synaptic AMPA receptor function.
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Furthermore, this mutation prevents the induction of long-term potentiation (LTP), the cellular mechanism underlying learning and memory formation. Together, our findings strongly suggest that this mutation contributes to the development of ID in this individual. This research demonstrates the importance of Rac1 in synaptic function and plasticity and contributes to a growing body of evidence pointing to dysregulation of actin polymerization at glutamatergic synapses as a contributing factor to ASD/ID. A de novo missense mutation in the P-loop region of Rac1 in an individual with severe intellectual disability (ID) is predicted to prevent Rac1 activation. (Top) Rac1 protein regions are indicated, starting with the N terminus: P-loop region, switch I and switch II. Location of a de novo ID-related missense mutation and control missense mutations are shown.