Desmosomal Antigens Are Not Recognized by the Majority of Pemphigus Autoimmune Sera

Sera from 7 patient with pemphigus vulgaris and both mouse and rabbit antisera against bovine epidermal desmosomes contained antibodies that bound to cell surface components of the spinous layer of bovine epidermis. The antidesmosomal sera show significant binding to purified desmosomal proteins in an enzyme-linked immunosorbent assay (ELISA). Two of 7 pemphigus sera bound to desmosomal protein-coated microtiter plates at low dilution titers. Two of 6 normal human sera also bound to desmosomal protein-coated microtiter plates at titers comparable to those of the pemphigus sera. Indirect immunofluorescent labeling of frozen sections of monkey esophagus revealed striking differences in the distribution of pemphigus antigens and desmosomal constituents. Pemphigus antisera produced rather uniform fluorescence around the borders of spinous cells of the esophageal epithelium, while anti-desmosomal antibodies bound in a punctate pattern. Anti-desmosomal antibodies labeled cells of the basal layer in a strongly punctate pattern. Only 1 pemphigus serum appreciably labeled basal cells. Two of 3 anti-desmosomal antisera bound avidly in the upper differentiating layers of the epithelium. Pemphigus antibodies did not. Pemphigus sera that reacted with desmosomal proteins in ELISA were absorbed by affinity chromatography on immobilized desmosomal proteins. This treatment did not alter the immunofluorescent labeling patterns produced by these sera. From these results we conclude that the pemphigus autoantibodies studied here bind to epithelial cell surface antigens which are distinguishable from the structural components of desmosomes

Immobilization of Fission Iodine by Reaction with a Fullerene Containing Carbon Compound and Insoluble Natural Matrix

Observations related to the oxidation of iodide to iodine (I2) or hypoiodic acid (HIO) by MnO2 were continued. The formation of triiodide presumable involves the adsorption of iodide onto the MnO2 surface (perhaps displacing a surface hydroxyl group). The iodide should be subsequently oxidized and released back into solution as IOH or I2, which rapidly forms I3 -. The kinetic data has been modeled as a first order process. First order rate constants have been obtained for the formation of iodine in the presence of MnO2. The increase in iodide oxidation rates with MnO2 concentration is evident in the data. The reaction rate increases with iodide concentration although the dependence is not first order (an order of 1.4 appear to fit the data). The oxidation rate also increases with temperature and has a apparent activation energy of 16.2 kJ/mol

Immobilization of Fission Iodine by Reaction with a Fullerene Containing Carbon Compound and Insoluble Natural Organic Matrix

The recovery of iodine released during the processing of used nuclear fuel poses a significant challenge to the transmutation of radioactive iodine. During the first year of this program we have examined the potential of Fullerene Containing Carbon compounds (FCC) developed by KRI, and natural organic matter (NOM) as sorbents for iodine released during the reprocessing of nuclear fuel. This work involved the development of bench-scale testing of the FCC and NOM material in a simulated process off-gas environment. During the first two quarters of this program we explored various analytical methods available for measurement of iodine, iodide, and iodate. We reproduced an analytical method proposed by Mishra et al., 2000 for measurement of trace levels of iodide and iodine in aqueous solution. Iodine or hypoiodic acid reacts with N,N-dimethylanaline to form p-iododimethylaniline. Iodide can be measured after selective oxidation of iodide with 2-iodosobenzoate to produce active iodine that is subsequently reacted with N,Ndimethylaniline. The product p-iodo-N,N-dimethylaniline can be quantified by GC/MS. This method gave excellent results in dilute aqueous solutions however; we did encounter some interference in the presence of NOM. The method should still be useful for quantifying low levels on iodine released by FCC or other sorbent materials

Immobilization of Fission Iodine by Reaction with a Fullerene Containing Carbon Compound and Insoluble Natural Matrix

The stability of the association of iodine with FCC and NOM products were studied. Product distributions for the various matrices under various reaction conditions were examined in order to maximize the binding of iodine. The recovery of the iodine from the sequestration matrices was also examined, along with the conversion of the iodine to matrices more suitable for geological storage and/or use as transmutation targets. The following are the specific research objectives and goals: Develop bench-scale experimental set-up and procedures for simulating plutonium extraction process (PUREX) head-end vapor phase. Develop experimental procedures for evaluating iodine sequestering methods using bench-scale procedures. Develop FCC bearing material as potential iodine sequestration matrix. Determine binding of iodine to FCC and NOM. Examine alternate iodine sequestration matrices using techniques developed for FCC and NOM studies. Examine the effect of reaction conditions on binding. Elucidate the nature of the reaction products (volatile, hydrophobic, soluble, insoluble). Develop methodology and host matrix for converting sequestered iodine to solid matrix for evaluation as transmutation target and/or disposal matrix. Examine recovery of iodine from sequestration matrices

Intraarterial transplantation of human umbilical cord blood mononuclear cells is more efficacious and safer compared with umbilical cord mesenchymal stromal cells in a rodent stroke model

INTRODUCTION: Stroke is the second leading cause of death worldwide, claims six lives every 60 seconds, and is a leading cause of adult disability across the globe. Tissue plasminogen activator, the only United States Food and Drug Administration (FDA)-approved drug currently available, has a narrow therapeutic time window of less than 5 hours. In the past decade, cells derived from the human umbilical cord (HUC) have emerged as a potential therapeutic alternative for stroke; however, the most effective HUC-derived cell population remains unknown. METHODS: We compared three cell populations derived from the human umbilical cord: cord blood mononuclear cells (cbMNCs); cord blood mesenchymal stromal cells (cbMSCs), a subpopulation of cbMNCs; and cord matrix MSCs (cmMSCs). We characterized these cells in vitro with flow cytometry and assessed the cells’ in vivo efficacy in a 2-hour transient middle cerebral artery occlusion (MCAo) rat model of stroke. cbMNCs, cbMSCs, and cmMSCs were each transplanted intraarterially at 24 hours after stroke. RESULTS: A reduction in neurologic deficit and infarct area was observed in all three cell groups; however, this reduction was significantly enhanced in the cbMNC group compared with the cmMSC group. At 2 weeks after stroke, human nuclei-positive cells were present in the ischemic hemispheres of immunocompetent stroke rats in all three cell groups. Significantly decreased expression of rat brain-derived neurotrophic factor mRNA was observed in the ischemic hemispheres of all three cell-treated and phosphate-buffered saline (PBS) group animals compared with sham animals, although the decrease was least in cbMNC-treated animals. Significantly decreased expression of rat interleukin (IL)-2 mRNA and IL-6 mRNA was seen only in the cbMSC group. Notably, more severe complications (death, eye inflammation) were observed in the cmMSC group compared with the cbMNC and cbMSC groups. CONCLUSIONS: All three tested cell types promoted recovery after stroke, but cbMNCs showed enhanced recovery and fewer complications compared with cmMSCs

Leelanau County Inland Lakes Project

Master of ScienceLandscape ArchitectureUniversity of Michiganhttp://deepblue.lib.umich.edu/bitstream/2027.42/114606/2/39015043175614.pd

Meningeal Mast Cells as Key Effectors of Stroke Pathology

Stroke is the leading cause of adult disability in the United States. Because post-stroke inflammation is a critical determinant of damage and recovery after stroke, understanding the interplay between the immune system and the brain after stroke holds much promise for therapeutic intervention. An understudied, but important aspect of this interplay is the role of meninges that surround the brain. All blood vessels travel through the meningeal space before entering the brain parenchyma, making the meninges ideally located to act as an immune gatekeeper for the underlying parenchyma. Emerging evidence suggests that the actions of immune cells resident in the meninges are essential for executing this gatekeeper function. Mast cells (MCs), best known as proinflammatory effector cells, are one of the long-term resident immune cells in the meninges. Here, we discuss recent findings in the literature regarding the role of MCs located in the meningeal space and stroke pathology. We review the latest advances in mouse models to investigate the roles of MCs and MC-derived products in vivo, and the importance of using these mouse models. We examine the concept of the meninges playing a critical role in brain and immune interactions, reevaluate the perspectives on the key effectors of stroke pathology, and discuss the opportunities and challenges for therapeutic development