Years before the major events that are tied to the New Left in American collective memory, Bay Area college students’ protests against the House Un-American Activities Committee garnered national media attention for their perceived radicalism in the face of the federal government. Student protesters’ altercation with police at San Francisco City Hall in May of 1960 became a turning point at which the Old Left, New Left, and McCarthyism converged, providing valuable insight into the transition of broad leftist activism from union-based to direct action protest. Through secondary sources including histories of early student protest as well as student newspapers, government publications, supporting organizations’ communications, and oral histories from participants, I construct a timeline of the challenges early student activists faced. This critical angle centers how these protests’ complicate the historical understanding of the university as the postwar institutional mediator for left-wing protest and radicalism, thereby revealing the disparities and power relations between students, professors, and administrators in the pursuit of their respective political agendas. This perspective, therefore, challenges the prevailing notion of universities as a natural partner of progressive social movements by emphasizing the institutional obstacles and inadequacies that restrict student political activism and expression.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19 and can result in preterm birth or severe disease or death in the mother. The research objective was to quantify the SARS-CoV-2 viral load in placental tissue and evaluate whether the placenta mounts an antiviral innate immune response. Furthermore, the study seeks to understand whether the timing of a COVID-19 infection during pregnancy correlates with viral load at the time of delivery and placental pathology. I, along with the two research technicians I am working closely with, hypothesize that a SARS-CoV-2 infection modulates the placental innate immune pathway in pregnant women and result in high viral loads in the context of placental pathology. The virus may amplify or dampen the innate immune response, significantly impacting viral clearance and potentially inducing substantial injury to maternal and fetal tissue. In the study, I helped extract RNA from two tissue types in the placenta, chorionic villous tissue and chorioamniotic membranes, from pregnant women with and without COVID-19 at different trimesters. I have begun to extract RNA, synthesize complementary DNA (cDNA), and perform quantitative polymerase chain reaction (qPCR) to quantify the viral load of SARS-CoV-2 per mg of tissue. In SARS-CoV-2 positive samples, I have also begun to quantify the relative gene expression of ifnb, mxa, ifit1, and il6, which will allow my team and I to evaluate the innate immune response. Our preliminary results indicate a low, but significant frequency of SARS-CoV-2 in placental tissues with rare high viral loads associated with a significant IL-6 response. I will help analyze our data through visual graphs and statistical analysis once the data is uploaded to the lab’s database. This project will not only improve our understanding of pregnancy pathologies, but also make significant strides in what is known about SARS-CoV-2’s impact on pregnancy health.

Plants face an enormous number of environmental stressors, including agriculturally important pests and pathogens. To defend against these biotic stressors, plants rely on pattern recognition receptors (PRRs), which are cell surface proteins that recognize conserved, non-self molecules indicative of attack or infection and initiate pattern triggered immunity (PTI) signaling pathways to mount defense responses. Recently, the first PRR involved in immunity against herbivorous pests was discovered in legumes. INR, a leucine-rich repeat receptor-like protein, mediates defense responses to inceptin, a peptide found in the oral secretions of caterpillars. To better understand the structural aspects of INR that are necessary for its ability to bind to inceptin and associate with downstream signaling components, I am developing a reporter system to screen INR variants to identify mutations that affect its function as a PRR. I have generated several different reporter constructs driving luciferase expression with promoter regions of genes found to be upregulated by inceptin when INR is transgenically expressed in the model organism Nicotiana benthamiana. These constructs vary in strength of expression but only one promoter region shows inducibility by inceptin. However, several constructs also show responses to a different immune elicitor, a peptide fragment of bacterial flagellin, which suggests that these constructs could be used as markers of PTI in plants more broadly. Robust reporters of PTI would not only be useful in understanding the structure and function of INR but may also enable further studies that will inform engineering practices to improve crop resistance to pests and pathogens.