June Jordan Interview : 09-24-1981

Interview of June Jordan at the Brockport Writers Forum on September 24, 1981. Ms. Jordan was interviewed by Adriane Livingston, Mary Elsie Robertson and Peter Marchant. The tape of the interview can be seen at http://digitalcommons.brockport.edu/writers_videos/19/

June Jordan: 09-24-1981

June Jordan was a poet and former professor of English at Stony Brook University. She begins the interview by reading her poem,“A Poem about Intelligence for My Brothers and Sisters.” She continues the interview by discussing how she first became a poet, and talks about her own political poetry and political poetry as a genre. She then talks about the situation in South Africa during the time period of this interview. Jordan briefly touches on her future literary plans and her contribution to literature as a black female writer, and ends the interview by discussing her criticism with the feminist movement.https://digitalcommons.brockport.edu/writers_videos/1019/thumbnail.jp

Capturing Heat from Spent Nuclear Fuel

ME450 Capstone Design and Manufacturing Experience: Winter 2021Spent Nuclear Fuel can be placed in dry cask storage, where it emits waste heat into the atmosphere. Our sponsor, Dr. Marianna Coulentianos, identified an opportunity to capture this heat for a beneficial application. Our team evaluated the feasibility of our sponsor’s previously proposed solutions and designed a system that could transfer heat from the dry cask. We focused specifically on quantifying the amount of heat that would be available for a therothecial application. In order to determine how much heat would theoretically be available, we constructed both mathematical and computational simulations of heat transfer through a duct system. The system we propose includes a square funnel feature at the cask interface, connected to a round, rigid duct system extending over the perimeter fence. It was observed that the outlet temperature of our proposed system is around 36-65℃, which we determined is most suitable for a greenhouse application. We calculated a return on investment of 5 years by growing tomatoes in a greenhouse of 1800 ft2. We are confident that our design is feasible and does not violate any regulations set forth by the Nuclear Regulatory Commission. However, more analysis is needed to further examine discrepancies between field data and our assumptions, as well as the scalability of our proposed solution. We also considered the social context of this solution. Eating fruits and vegetables grown on a nuclear site is likely to cause skepticism around our solution. While we believe that the radiation levels of this waste heat are too low to realistically affect horticultural applications, all food that is intended for human or animal consumption in the United States must register with the FDA before beginning these activities.Dr. Marianna Coulentianos: UM Mechanical Engineering Departmenthttp://deepblue.lib.umich.edu/bitstream/2027.42/167636/1/Team_17-Capturing_Heat_from_Spent_Nuclear_Fuel.pd

Engineering HIV-Resistant Human CD4+ T Cells with CXCR4-Specific Zinc-Finger Nucleases

HIV-1 entry requires the cell surface expression of CD4 and either the CCR5 or CXCR4 coreceptors on host cells. Individuals homozygous for the ccr5Δ32 polymorphism do not express CCR5 and are protected from infection by CCR5-tropic (R5) virus strains. As an approach to inactivating CCR5, we introduced CCR5-specific zinc-finger nucleases into human CD4+ T cells prior to adoptive transfer, but the need to protect cells from virus strains that use CXCR4 (X4) in place of or in addition to CCR5 (R5X4) remains. Here we describe engineering a pair of zinc finger nucleases that, when introduced into human T cells, efficiently disrupt cxcr4 by cleavage and error-prone non-homologous DNA end-joining. The resulting cells proliferated normally and were resistant to infection by X4-tropic HIV-1 strains. CXCR4 could also be inactivated in ccr5Δ32 CD4+ T cells, and we show that such cells were resistant to all strains of HIV-1 tested. Loss of CXCR4 also provided protection from X4 HIV-1 in a humanized mouse model, though this protection was lost over time due to the emergence of R5-tropic viral mutants. These data suggest that CXCR4-specific ZFNs may prove useful in establishing resistance to CXCR4-tropic HIV for autologous transplant in HIV-infected individuals

Antigen-Specific Blocking of CD4-Specific Immunological Synapse Formation Using BPI and Current Therapies for Autoimmune Diseases

This is the peer reviewed version of the following article: Manikwar, P., Kiptoo, P., Badawi, A. H., Büyüktimkin, B. and Siahaan, T. J. (2012), Antigen-specific blocking of CD4-Specific immunological synapse formation using BPI and current therapies for autoimmune diseases. Med Res Rev, 32: 727–764. doi:10.1002/med.20243, which has been published in final form at http://doi.org/10.1002/med.20243. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving.In this review, we discuss T-cell activation, etiology, and the current therapies of autoimmune diseases (i.e., MS, T1D, and RA). T-cells are activated upon interaction with antigen-presenting cells (APC) followed by a “bull’s eye”-like formation of the immunological synapse (IS) at the T-cell–APC interface. Although the various disease-modifying therapies developed so far have been shown to modulate the IS and thus help in the management of these diseases, they are also known to present some undesirable side effects. In this study, we describe a novel and selective way to suppress autoimmunity by using a bifunctional peptide inhibitor (BPI). BPI uses an intercellular adhesion molecule-1 (ICAM-1)-binding peptide to target antigenic peptides (e.g., proteolipid peptide, glutamic acid decarboxylase, and type II collagen) to the APC and therefore modulate the immune response. The central hypothesis is that BPI blocks the IS formation by simultaneously binding to major histocompatibility complex-II and ICAM-1 on the APC and selectively alters the activation of T cells from TH1 to Treg and/or TH2 phenotypes, leading to tolerance