85 research outputs found
Losses of NG2 and NeuN immunoreactivity but not astrocytic markers during early reperfusion following severe focal cerebral ischemia
No full textDiane R. Lee, Stephen C. Helps, Ian L. Gibbins, Michael Nilsson, Neil R. Sim
Testing Theories of Discrimination: Evidence from "Weakest Link"
No full textIn most settings, it is difficult to measure discrimination, and even more challenging to distinguish between competing theories of discrimination (taste-based versus information-based). Using contestant voting behavior on the television game show Weakest Link, one can in principle empirically address both of these questions. On the show, contestants answer questions and vote off other players, competing for a winner-take-all prize. In early rounds, strategic incentives encourage voting for the weakest competitors. In later rounds, the incentives reverse, and the strongest competitors become the logical target. Controlling for other observable characteristics including the number of correct answers thus far, both theories of discrimination predict that in early rounds, excess votes will be made against groups targeted for discrimination. In later rounds, however, taste-based models predict continued excess votes, whereas statistical discrimination predicts fewer votes against the target group. Empirically, I find some evidence of information-based discrimination towards Hispanics (i.e., other players perceive them as having low ability) and taste-based discrimination against older players (i.e., other players treat them with animus). There is little in the data to suggest discrimination against women and Blacks.
Fluorocitrate-mediated astroglial dysfunction causes seizures
No full textPublished in Journal of Neuroscience Research, 2003; 74 (1):160-166 at www.interscience.wiley.comA role for astroglia in epileptogenesis has been hypothesised but is not established. Low doses of fluorocitrate specifically and reversibly disrupt astroglial metabolism by blocking aconitase, an enzyme integral to the tricarboxylic acid cycle. We used cerebral cortex injections of fluorocitrate, at a dose that we demonstrated to inhibit astroglial metabolism selectively, to determine whether astroglial disturbances lead to seizures. Rats were halothane-anesthetized, and 0.8 nmol of sodium fluorocitrate was injected into the cerebral cortex. Extradural electroencephalogram (EEG) electrodes were implanted, after which the anesthesia was ceased and the animals were observed. In all experiments, 14 of 15 fluorocitrate-treated animals exhibited epileptiform EEG discharges, with some animals exhibiting convulsive seizures. Discharges commenced as early as 30 min postfluorocitrate injection. Intraperitoneal octanol, but not halothane by inhalation, given to test the possible participation of gap junctions in EEG discharge generation, blocked or delayed the occurrence of discharges after fluorocitrate. These results indicate that focal cerebrocortical astroglial dysfunction leads to focal epileptiform discharges and sometimes to convulsive seizures and that the process possibly depends on effects mediated by gap junctions.John O. Willoughby, Lorraine Mackenzie, Marita Broberg, Anna E. Thoren, Andrei Medvedev, Neil R. Sims, Michael Nilsso
Big Ridge - early Jackson County school
No full textThis photograph shows a class standing in front of Big Ridge School in Glenville, North Carolina. After the school burned in 1922, the Board of Education ordered that the school be rebuilt at an April 1923 meeting. Mabel Edwards was the school principal from 1924 to 1925. Information on the school’s consolidation or closing is unknown. The following are the names of identified students and teachers in this photograph: (first row) J. B. Galloway, Raymond Wilson, Alvin Nicholson, Earnest Pressly, Neil Burgas ; (second row) Eva Brown (teacher), Bessie Hooper, Matthew Wilson, Cassie Wilson, Emma Jamison, Irma Henderson ; (third row) Della Wilson, Ollie Bryson, Rose Henson, Emma Lonniz, Effie Bryson, Lula Wilson, Lizzie Wilson, Elsie Monteith ; (fourth row) Sam Wilson, Earnest Wilson, [Weaver] Wilson, Edd Wilson, Bert Sims, Tom Moss, Ruff Lusk, [Dyre] Lusk, Walter Wilson, Walter Monteith, Lawton Henderson, John Bird (teacher on the end)
Inhibition of Nitric Oxide Synthase with 7-Nitroindazole does not Modify Early Metabolic Recovery Following Focal Cerebral Ischemia in Rats
No full textNitric oxide has been strongly implicated in the development of tissue infarction in response to focal cerebral ischemia. Nitric oxide and its derivatives can inhibit components of the electron transport chain, providing a likely target for these substances in ischemic and post-ischemic brain. Lactate content is increased during post-ischemic reperfusion in tissue destined to become infarcted, consistent with impairment of mitochondrial respiration. To investigate the possible involvement of nitric oxide in generating these changes, we have tested the effect of 7-nitroindazole, a nitric oxide synthase (NOS) inhibitor, on the content of lactate and other metabolites during early reperfusion following temporary focal ischemia. This treatment inhibited total NOS by approximately 50%. However, the treatment did not significantly affect the marked increases in lactate in post-ischemic brain nor did it alter the recovery of other energy-related metabolites. These findings indicate that inhibition of oxidative metabolism is probably not the primary site of the deleterious effects of nitric oxide and derivatives during early post-ischemic reperfusion
Increased mitochondrial permeability in response to intrastriatal N-methyl-D-aspartate : detection based on accumulation of radiolabel from[3h]deoxyglucose
No full text233 SPRING ST, NEW YORK, USA, NY,
1001
Highly selective and prolonged depletion of mitochondrial glutathione in astrocytes markedly increases sensitivity to peroxynitrite
No full text11 DUPONT CIRCLE, NW, STE 500, WASHINGTON,
USA, DC, 2003
Mitochondria, oxidative metabolism and cell death in stroke
No full textAbstractStroke most commonly results from occlusion of a major artery in the brain and typically leads to the death of all cells within the affected tissue. Mitochondria are centrally involved in the development of this tissue injury due to modifications of their major role in supplying ATP and to changes in their properties that can contribute to the development of apoptotic and necrotic cell death. In animal models of stroke, the limited availability of glucose and oxygen directly impairs oxidative metabolism in severely ischemic regions of the affected tissue and leads to rapid changes in ATP and other energy-related metabolites. In the less-severely ischemic “penumbral” tissue, more moderate alterations develop in these metabolites, associated with near normal glucose use but impaired oxidative metabolism. This tissue remains potentially salvageable for at least the first few hours following stroke onset. Early restoration of blood flow can result in substantial recovery of energy-related metabolites throughout the affected tissue. However, glucose oxidation is markedly decreased due both to lower energy requirements in the post-ischemic tissue and limitations on the mitochondrial oxidation of pyruvate. A secondary deterioration of mitochondrial function subsequently develops that may contribute to progression to cell loss. Mitochondrial release of multiple apoptogenic proteins has been identified in ischemic and post-ischemic brain, mostly in neurons. Pharmacological interventions and genetic modifications in rodent models strongly implicate caspase-dependent and caspase-independent apoptosis and the mitochondrial permeability transition as important contributors to tissue damage, particularly when induced by short periods of temporary focal ischemia
Isolation of mitochondria from rat brain using Percoll density gradient centrifugation
No full textLondon U
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