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.

 Alzheimer’s disease (AD) is a complex and common neurodegenerative disease in humans. It is diagnosed by the presence of A beta amyloid plaques and tau tangles in the brain during autopsy, decades after neuropathology has developed. Early diagnosis is still not definitive and contributes to the inability to successfully treat the disease at an early stage. Generally, animal models are not reliable for preclinical studies since lower mammals, including laboratory rodents and nonhuman primates, pet dogs and domestic livestock do not naturally develop AD. The reason is based on conformational differences in amyloid precursor and tau proteins. We have recently observed one exception to this list of mammals- the aging pet cat. Formalin fixed paraffin embedded brain sections from ten 16 to18-year-old pet cats obtained from a regional veterinary teaching hospital were stained with antibodies 6E10 and AT8 specific for A beta and phosphorylated tau using standard immunohistochemistry procedures for diagnosing human AD. One cat showed robust tau tangles and moderate amyloid plaques, while a second cat showed moderate tau tangles and mild amyloid plaques. Brains from additional cats need to be examined for AD neuropathology but this preliminary observation suggests old pet cats develop AD. Since pet cats share the same environment as humans, clinical studies to search for ways of early diagnosis and treatment of this naturally occurring disease in cats will have a huge impact on the translational implications for early diagnosis and intervention studies in human AD.

Acute respiratory distress syndrome (ARDS) is a significant cause of morbidity and mortality in older people. ARDS is initially mediated by an acute lung injury (ALI) response. Studies are needed to investigate why aging increases the risk for more severe ALI and complications assoicated with ALI. Animal models are useful for these types of investigations but most studies use young animals and therefore do not replicate an aging environment and fail to provide valid translational information. The purpose of this pilot study was to determine the pulmonary response and serum cytokine levels in old mice exposed to lipopolysaccharide (LPS), designed to induce ALI. Twenty C57BL/6 mice, 22 months of age, were exposed to 800 ng LPS in 50 ul of saline or saline alone by endotracheal instillation. Two days later, mice were euthanized and serum, lung and other tissues were collected. Serum was tested by ELISA for inflammatory cytokines TNFalpha and IL-6. Lungs were formalin fixed for H and E staining, and slides were read by a veterinary pathologist. Serum TNFalpha and IL-6 were both significantly increased in LPS treated mice compared to baseline and saline controls. Lung pathology consisted of an acute response of proteinaceous exudate flooding alveolar spaces, inflammatory cells within interstitial and alveolar spaces, and inflammatory cells surrounding and within small blood vessels. Additional studies are needed to confirm the utility of the model but this preliminary observation suggests that LPS-induced ALI in old mice might enable more valid investigations into pathogenesis and interventions associated with ARDS and respiratory afflictions caused by SARS-Co-V2 and related virus infections in older people.