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How brain functions in the distorted ischemic state before and after reperfusion is unclear. It is also uncertain whether there are any indicators within ischemic brain that could predict surgical outcomes. To alleviate these issues, we applied individual brain connectome in chronic steno‐occlusive vasculopathy (CSOV) to map both ischemic symptoms and their postbypass changes. A total of 499 bypasses in 455 CSOV patients were collected and followed up for 47.8 ± 20.5 months. Using multimodal parcellation with connectivity‐based and pathological distortion‐independent approach, areal MR features of brain connectome were generated with three measurements of functional connectivity (FC), structural connectivity, and PageRank centrality at the single‐subject level. Thirty‐three machine‐learning models were then trained with clinical and areal MR features to obtain acceptable classifiers for both ischemic symptoms and their postbypass changes, among which, 11 were deemed acceptable (AUC > 0.7). Notably, the FC feature‐based model for long‐term neurological outcomes performed very well (AUC > 0.8). Finally, a Shapley additive explanations plot was adopted to extract important individual features in acceptable models to generate "fingerprints" of brain connectome. This study not only establishes brain connectomic fingerprint databases for brain ischemia with distortion, but also provides informative insights for how brain functions before and after reperfusion. [ABSTRACT FROM AUTHOR]

Internet extends the reach of existing laboratory and training infrastructure to beyond the walls of such facilities. Though nothing can replace the hands-on experience in a laboratory; a carefully developed web-based digital lab may be the next best thing. In some cases, there may be benefits associated with a "distance laboratory" that are usually not available in a conventional lab. Due to radiation environment and very high cost of some labs--for example, nuclear research reactors--there exists a need to develop web-based systems that can access the experiments being conducted in a radiation measurement lab or the reactor and make it available in a virtual laboratory. These systems should be inexpensive, easily installable, allow interactive audio/video communication as well as remote access (or sharing) of data in real-time. We here report the development of a real-time, distance lab module that is being implemented in the Department of Nuclear, Plasma and Radiological Engineering at the University of Illinois. This internet-based system allows remote personnel to watch the experiments and personnel performing the experiments, acquire data, and interact (audio and video) with on-site personnel. Data are broadcasted in real time in text as well as graphical format--the same format used to display the data on site. Moreover, use of LabVIEW's "remote front panel" feature allows communications between the local lab and remote client so that remote client, if permitted, can obtain part or full control of the experiments.

Aim: The class I histone deacetylases (HDACs) implicate in microglial heterogenization and neuroinflammation following Intracerebral hemorrhage (ICH). Ferroptosis has also been reported in the ICH model. However, the relationship between HDAC1/2's role in microglial heterogenization and neuronal ferroptosis remains unclear. Methods: In both in vivo and in vitro models of ICH, we used Romidepsin (FK228), a selective HDAC1/2 inhibitor, to investigate its effects on microglial heterogenization and neuronal ferroptosis. In the in vitro ICH model using Hemin, a transwell system was utilized to examine how microglia‐driven inflammation and ICH‐triggered neuronal ferroptosis interact. Immunostaining, Western blotting and RT‐qPCR were used to evaluate the microglial heterogenization and neuronal ferroptosis. Microglial heterogenization, neuronal ferroptosis, and neurological dysfunctions were assessed in vivo ICH mice model performed by autologous blood injection. Results: HDAC1/2 inhibition altered microglial heterogenization after ICH, as showing the reducing neuroinflammation and shifting microglia towards an anti‐inflammatory phenotype by immunostaining and qPCR results. HDAC1/2 inhibition reduced ferroptosis, characterized by high ROS and low GPx4 expression in HT22 cells, and reduced iron and lipid deposition post‐ICH in vivo. Additionally, the Nrf2/HO1 signaling pathway, especially acetyl‐Nrf2, activated in the in vivo ICH model due to HDAC1/2 inhibition, plays a role in regulating microglial heterogenization. Furthermore, HDAC1/2 inhibition improved sensorimotor and histological outcomes post‐ICH, offering a potential mechanism against ICH. Conclusion: Inhibition of HDAC1/2 reduces neuro‐ferroptosis by modifying the heterogeneity of microglia via the Nrf2/HO1 pathway, with a particular focus on acetyl‐Nrf2. Additionally, this inhibition aids in the faster removal of hematomas and lessens prolonged neurological impairments, indicating novel approach for treating ICH. [ABSTRACT FROM AUTHOR]