Maia
Goel
Inflammatory response following TBI is implicated in post-traumatic epileptogenesis, although the exact pathway and mechanism remains unclear. The lifetime burden of both TBI and epilepsy are high, and especially when they are concurrent. Our study probed the expression of several proteins implicated in a proposed neural response pathway in groups of mice subjected to TBI, inflammation-causing agents, and both, across various time points. Ten mice were divided into four groups: sham (untreated), LPS-treated, TBI-injured, and LPS + TBI. Mice were first treated with LPS, if applicable, to induce inflammation. Mice were then injured with TBI at a 3mm displacement. Brain was fixed at time points of 3, 6, 9, and 24 hrs. Protein isolation and concentration assays were completed using these experimental animals at each time point. All results were compared to findings in control (sham/untreated) animals to account for the neurological ePects of surgical anesthesia. Findings included high BDNF expression at 3 and 9 hours in LPS-treated groups, as well as slightly elevated levels at 9 hours in the TBI-only group. IL1-Ra expression lingered at high levels for much longer in TBI + LPS mice than in TBI-only or LPS-only mice. AIF1 peaked at 6 hours in both TBI groups, but not in the LPS-only group. IKBa expression was relatively similar across groups, but all treated groups (TBI, LPS, and TBI + LPS) showed very high levels of pIKBa at 6 hours compared to controls. NFKB showed increased expression at 24 hours in both LPS-treated groups, and pNFKB spiked at 6 hours in all groups, especially LPS and LPS + TBI. LRP showed relatively consistent expression across all groups and time points. Expression of most all proteins was highest at 6 hours, except BDNF which peaked at 9 hours. These results provide potential insight into the regulation of inflammatory response following TBI and inflammation, including potential overlap and divergence in pathways. Establishing cell lines from fresh and frozen mouse lemur tissue
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Authors:
Maia Goel
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Complete, high-quality genomes exist for few species due to the complexity of sequencing areas containing complex repeated elements like telomeres and centromeres. This deficit needs to be addressed. Precise reference genomes-ideally, telomere-to-telomere (T2T) genomes-have the potential to significantly advance our understanding of all biological phenomena and the evolutionary processes that shape them. Mouse lemurs, an endangered clade of primates, are an ideal system to study the evolutionary processes aPecting the biological process of speciation, but a complete T2T reference genome for this or any other lemur clade does not yet exist. Creating a T2T reference genome requires a large amount of high-quality DNA, ideally from natural populations. Methods for collecting DNA from natural populations in Madagascar are enormously challenging for numerous reasons relating to the organisms and the challenges of working in the impoverished country of Madagascar. Thus, we must rely on lab-based technologies to overcome these challenges. In this study, we first adapted existing cell culture protocols to successfully culture mouse lemur cells and thereby amplify small amounts of available genetic material. Additionally, we are developing a protocol for tissue cryopreservation that can be reproduced under diPicult field conditions. This protocol will allow us to obtain frozen tissue with viable cells for cell cultures. To our knowledge, these protocols have never been established for lemur cells. Once completed, however, they can be adapted for the study of other non-model organisms and endangered species. Our work will ultimately shed light on mouse lemur speciation, resulting in one of few complete T2T genomes for a non-model organism, and further enabling future studies of Earth's endangered biota.
Source:
Duke University / 2024
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Co-authors:
Maia Goel