Political satire is often viewed as a form of indirect political expression commonly employed in authoritarian states like China. When social media is heavily regulated, satire serves as a rhetorical tool to circumvent censorship. However, satire might vary across various types of political discussion, including housing, unemployment, and the overwork culture. While prior research has extensively examined political satire and censorship in China, there is little research comparing how satire functions differently across political discussion themes. This study hypothesizes a correlation between themes of political discussion and the role and characteristics of satire in political discourse by analyzing content on Zhihu, a Chinese Q&A platform. Specifically, it examines (1) the correlation between discussion themes and stance to assess whether satire is a necessary feature for expressing dissent, (2) the prevalence of satire, measured by the proportion of satirical posts within each theme, and (3) the relationship between linguistic ambiguity and satire to determine whether ambiguity is a key strategy for evading censorship. The methodology consists of three main steps: (1) Construct a dataset by creating a random sample from a list of select political discussion themes and scraping the top discussion forums, recommended by the platform's algorithms, to ensure the sample reflects the overall user experience. (2) Qualitative text annotation based on the post's stance, ambiguity, and the presence of satire. (3) Applying natural language processing techniques to examine cross-topic variations in the use of satire and other rhetorical strategies. This approach facilitates a systematic exploration of how different types of public political discussions utilize satire to evade censorship. This research contributes to the broader understanding of political discourse under authoritarianism, offering insights into how citizens navigate the boundaries of permissible speech. 

The axon initial segment (AIS) plays a crucial role in maintaining neuronal excitability and action potential initiation. It is structurally and functionally plastic, adapting to pathological conditions such as traumatic brain injury (TBI). While microglia, the resident immune cells of the central nervous system, are known to respond to injury and influence neuronal function, their interactions with the AIS remain underexplored. This study aims to investigate whether microglia associate with and alter the AIS before and after TBI, contributing to potential changes in excitability. Using a transgenic mouse model with GFP-labeled microglia, brain tissue is stained for neurons (Nissl), microglia (GFP), and the AIS (Ankyrin G) followed by confocal microscopy to obtain high-resolution images to visualize microglial interactions with the AIS. Image J is utilized to quantify AIS length, fluorescence intensity, and microglial proximity. I hypothesize that TBI induces structural changes in the AIS, including shortening or fragmentation, and that microglial interaction may play a role in these alterations. Preliminary data suggest an increased microglial presence near the AIS after injury, potentially indicating a role in either AIS disruption or repair. By identifying how microglia interact with the AIS, this research contributes to our understanding of neuroinflammatory responses following TBI. These findings may have implications for therapeutic strategies aimed at preserving neuronal function after injury. Further studies will explore whether microglia mediate AIS remodeling through direct contact or secreted factors, offering insights into potential interventions for TBI-related neurological dysfunction.

Traumatic brain injury (TBI) can occur after experiencing an explosion or any external force to the head. TBIs are exceedingly common and frequently associated with some degree of behavioral and/or cognitive impairment. However, the underlying causes of these impairments are unknown. To bridge this gap in knowledge, our lab examines the pathology in brain regions that account for the nodes of networks important in cognitive and behavioral function, including the default mode/executive control and limbic/salience network respectively, in brain donors with a history of behavioral, cognitive, or mixed decline. Oligodendrocytes are glial cells in the brain that are important to the production of myelin. Injury to the brain can lead to their cell death. We aim to uncover whether TBI donors with cognitive, behavioral, or mixed decline have reduced amounts of oligodendrocyte in brain regions associated with such functions. To investigate this, slides of over 20 regions of the brain are stained with an antibody that marks oligodendrocytes, Olig2. The slides are then scanned with an Aperio slide scanner and imported to Halo image analysis software. Utilizing this software, I annotate the grey matter of these slides, so that the percentage of the area of staining can be determined for pixels in a specific intensity range. Preliminary results in 5 of the brain donors demonstrates no significant difference in the % staining of Olig2 across the brain regions regardless of clinical pattern of decline. Experiments will need to be conducted on controls of donor brains without TBI and on white matter, a region with higher amounts of oligodendrocytes that may function differently than oligodendrocytes in grey matter.

After traumatic brain injury (TBI), astrocytes can undergo distinct changes in function and morphology, termed astrogliosis. Astrocytes are important glial cells with roles in maintaining neural circuits. This astrogliosis can lead to maladaptive changes, inhibiting proper support of circuitry that might lead to hyperexcitability.  TBI is a risk factor for the development of epilepsy, and we wondered whether increased astrogliosis is present in cases that develop epilepsy compared to TBI without epilepsy. To assess this question, we examined astrogliosis in male brain donors with a remote history of TBI with and without post-traumatic epilepsy, as well as controls in a similar age range. Immunohistochemical staining for glial fibrillary acidic protein (GFAP), an astrocytic cytoskeleton protein, was used to visualize and quantify astrogliosis. The percentage area of staining was determined in both the orbitofrontal cortex (OFC), a region commonly vulnerable to TBI, as well as the thalamus, a region important in seizure spreading in the brain. Morphologic changes in astrocytes were analyzed with immunofluorescence staining for GFAP, using Sholl analysis to determine changes in astrocytic branching patterns in the OFC and the thalamus. Our results demonstrate increased astrogliosis in the thalamus and OFC in the post traumatic epilepsy group but not the TBI without epilepsy group compared controls. This supports our hypothesis that there is an association between post traumatic epilepsy and astrogliosis. Further research is needed to understand how astrogliosis might modify neural circuits to initiate or spread hyperexcitable activity associated with epilepsy.