Archiving the \u2780s: Feminism, Queer Theory, & Visual Culture

Archiving the \u2780s: Feminism, Queer Theory, & Visual Culture locates a shared genealogy of feminism and queer theory in the visual culture of 1980s American feminism. Gathering primary sources from grant-funded research in a dozen archives, I analyze an array of image-text media of women, ranging from well known creators like Gloria Anzaldúa, Alison Bechdel, and Nan Goldin, to little known ones like Roberta Gregory and Lee Marrs. In each chapter, I examine how each woman develops movement politics in her visual production, and I study the reception of their works in their communities of influence. Through studying hybrid visual rather than merely literary output, I explore the overlooked role of visual culture in feminist and LGBT social justice movements. In the first chapter, I review the transition period from the 1970s through the comics work of Roberta Gregory and Lee Marrs. Their early comics demonstrate the limitations of 1970s feminism, and I analyze how they develop their critiques in the 1980s in newly created comics series like Gay Comix (1980-1998). In the second chapter, I reconfigure the legacy of cartoonist Alison Bechdel as a grassroots activist through analyzing her participation as production coordinator of multiple grassroots periodicals across the 1980s. The third chapter resituates Chicana theorist Gloria Anzaldúa as a visual thinker and examines how she fuses race and sexuality in drawings that she would use to illustrate her own talks. I consider the importance of visual discourse to women of color feminism by evaluating the changing visual material in each version of her famed anthology, This Bridge Called My Back (1981, 1983, 2002, 2015). In the fourth chapter, I scrutinize the evolving politics of photographer Nan Goldin in her well-known The Ballad of Sexual Dependency slideshow and in her little-discussed curation of the controversial AIDS exhibit, Witnesses: Against Our Vanishing (1989). Through these artists’ visual production, I argue that the visual offers a more capacious form of feminism that embraces diversity, especially around issues of sexuality

Potential for Transcranial Laser or LED Therapy to Treat Stroke, Traumatic Brain Injury, and Neurodegenerative Disease

Near-infrared (NIR) light passes readily through the scalp and skull and a small percentage of incident power density can arrive at the cortical surface in humans.1 The primary photoreceptors for red and NIR light are mitochondria, and cortical neurons are exceptionally rich in mitochondria. It is likely that brain cells are ideally set up to respond to light therapy. The basic biochemical pathways activated by NIR light, e.g., increased adenosine-5’-triphosphate (ATP) production, and signaling pathways activated by reactive oxygen species, nitric oxide release, and increased cyclic adenosine monophosphate (AMP) all work together to produce beneficial effects in brains whose function has been compromised by ischemia, traumatic injury, or neurodegeneration. One of the main mechanisms of action of transcranial light therapy (TLT) is to prevent neurons from dying, when they have been subjected to some sort of hypoxic, traumatic, or toxic insult. This is probably because of light-mediated upregulation of cytoprotective gene products such as antioxidant enzymes, heat shock proteins, and anti-apoptotic proteins. Light therapy in vitro has been shown to protect neurons from death caused by methanol,2 cyanide or tetrodotoxin, 3 and amyloid beta peptide.4 There is also probably a second mechanism operating in TLT; increased neurogenesis. Neurogenesis is the generation of neuronal precursors and birth of new neural cells.5 Two key sites for adult neurogenesis include the subventricular zone (SVZ) of the lateral ventricles, and the subgranular layer (SGL) of the dentate gyrus in the hippocampus.6 Neurogenesis can be stimulated by physiological factors, such as growth factors and environmental enrichment, and by pathological processes, including ischemia and neurodegeneration.7 Adult neurogenesis (in the hippocampus particularly) is now recognized as a major determinant of brain function both in experimental animals and in humans. Neural progenitor cells in their niche in the SGL of the dentate gyrus give birth to newly formed neurons that are thought to play a role in brain function, particularly in olfaction and in hippocampal-dependent learning and memory. In small animal models neurogenesis can be readily detected by incorporation of bromodeoxyuridine (BrdU), injected before euthanasia, into proliferating brain cells. Increased neurogenesis after TLT, has been demonstrated in a rat model of stroke,9 and in the Hamblin laboratory after TLT for acute traumatic brain injury (TBI) in mice (W. Xuan, T. Ando, et al., unpublished data). These two mechanisms of action of TLT in ameliorating brain damage (prevention of neuronal death and increased neurogenesis) have motivated studies in both animals and humans for diverse brain disorders and diseases. TLT for acute stroke is the most developed,10 but acute TBI has also been shown to benefit from TLT.11 These areas are reviewed further.United States. Dept. of Veterans Affairs. Medical Research ServiceNational Institutes of Health (U.S.) (Grant R01AI50875)Center for Integration of Medicine and Innovative Technology (DAMD17-02-2-0006)United States. Dept. of Defense. Congressionally Directed Medical Research Programs ( Program in TBI W81XWH-09-1-0514)United States. Air Force Office of Scientific Research (F9950-04-1-0079