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Terry Lichtor and George J. Dohrmann

I t has been recognized for some time that cancer cells have an impaired respiratory capacity associated with elevated rates of glycolysis. 17 This has been found to be related in most cases to rapid tumor growth with increased glucose uptake coupled with a reduced number of mitochondria per cell; in particular, rapidly growing tumors almost without exception have a reduction in mitochondria of 50% or more. 13 Although most tumor mitochondria appear to have a normal complement of electron-transport chain components, several hepatoma lines have been found to

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Fengming Lan, Qing Qin, Huiming Yu and Xiao Yue

accompanied by multiple genetic changes, including alterations in microRNAs (miRNAs) that participate in apoptosis, DNA repair, and cell cycle control. 2 The abnormal expression of miRNAs leads to changes in cellular and genetic factors related to treatment responses, which may explain the cellular phenotypes of radiotherapy resistance. Thus, abnormal miRNA expression may be an important factor influencing the response of GBM to treatment. A high rate of glycolysis is a common feature of various types of cancer cells. Glycolytic reprogramming is characterized by increased

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Energy state and glycolysis in human cerebral edema

The application of a new freeze-stop technique

Peter Schmiedek, Alexander Baethmann, Gunter Sippel, Wolfgang Oettinger, Robert Enzenbach, Frank Marguth and Walter Brendel

of edematous human brain have been undertaken. Kirsch and Leitner 24 studied the glycolysis of human gray and white matter in vitro ; Reulen, et al. , 39 using neurosurgical patients, studied adenine nucleotides, phosphocreatine, lactic and pyruvic acid concentrations in combination with electrolyte and water content measurements in perifocal and more distant cortical areas. Olesen 34 determined total CO 2 lactate, and pyruvate concentrations in biopsy specimens of perifocal edematous areas. The freeze-stop methods generally in use are perfectly suitable

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Paul D. Chumas, James M. Drake, Marc R. Del Bigio, Marcia Da Silva and Ursula I. Tuor

consistent with mild cerebral ischemia and delayed myelination (unpublished data). In view of these changes, we decided to examine whether anaerobic glycolysis was present in this animal model by studying local cerebral glucose utilization (CMR glu ) and oxidative metabolism (cytochrome oxidase) in control, hydrocephalic, and shunted hydrocephalic animals. Sections taken for autoradiography were subsequently prepared for histological examination so that the pattern of glucose utilization and histological findings could be directly compared. Materials and Methods

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Matthew Womeldorff, David Gillespie and Randy L. Jensen

transcription of > 100 genes involved in various cellular survival pathways, including those involved in glucose uptake, glycolysis, and angiogenesis. (Figure reproduced with permission of the Department of Neurosurgery, University of Utah.) Under hypoxic conditions (1%–2% O 2 ), both of the above-mentioned regulatory mechanisms of HIF-1α become inhibited by substrate (O 2 ) deprivation. Furthermore, sumoylation of lysine residues 477 and 391 by the small ubiquitin-like modifier (SUMO)-1 enhances HIF-1α stability and upregulation, further augmenting its transcriptional

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Wolff M. Kirsch and John W. Leitner

T he purpose of this investigation was to compare the glycolytic response of malignant astrocytomas to that of the human brain (white matter) when incubated under anaerobic conditions. Cerebral tissue rapidly reacts to oxygen deprivation by degrading glucose and glycogen to form an equivalent amount of lactate (two equivalents of lactate per equivalent of hexose expended). 3 Glycolysis in the mammalian brain thus follows a well-defined anaerobic system (the Embden-Meyerhof pathway) to provide a short-term emergency source of energy for the ischemic brain

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Reduction of cellular energy requirements

Screening for agents that may protect against CNS ischemia

Eric L. Zager and Adelbert Ames III

issue of cellular metabolic requirements, we have used an isolated preparation of organized adult mammalian central nervous system (CNS) tissue (rabbit retina) maintained in a miniature heart-lung apparatus. This experimental preparation has allowed us to monitor metabolic parameters (oxygen consumption and glycolysis) as well as electrophysiological function. We have found this system to be relatively simple and highly reproducible, and have used it to screen agents of potential benefit to ischemic CNS cells. Our screening to date has disclosed a number of agents

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Kenneth R. Wagner, Guohua Xi, Ya Hua, Marla Kleinholz, Gabrielle M. de Courten-Myers and Ronald E. Myers

throughout, fail to show increased blood lactate levels (data not shown), and have ipsilateral but distant and contralateral white and gray matter lactate levels that are equal to control values ( Figs. 4 and 7 ). It has been suggested that elevated white matter lactate levels in both infusion and cold-injury edema 34 and in collagenase-induced ICH 23 are caused by hypoxia-induced stimulations of glycolysis. This hypoxia is believed to result from edema-induced expansion of the extracellular space that increases the distance of white matter axons and cells from their

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Jack M. Fein

periarteriolar catecholamines and their receptors. 14, 36, 37, 47, 52 Although such lines of investigation should continue, it is expected that a more holistic view of the pathophysiology of SAH may lead to increasing attention to the complex interplay between intermediary metabolism and flow and thereby afford a more complete perspective for therapy. The preserved energy stores and the depressed glycolysis noted in this study may be the metabolic correlate of a protective response to SAH. Such an interval may represent the safe time during which the encephalopathy noted may

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Daniel R. LeMay, Gerald B. Zelenock and Louis G. D'Alecy

Several factors may play an important role in hyperglycemic exacerbation of neurological deficit, and tissue lactate accumulation has been suggested as a major contributor. 7, 15, 20, 24, 28 In the present study, we examined the role of glucose metabolism occurring after the hexokinase step of glycolysis and the tricarboxylic acid (TCA) cycle on hyperglycemic exacerbation of neurological deficit. Iodoacetate was used to block an intermediate step of glycolysis and dichloroacetate was used to increase the flux of glycolysis metabolites into the TCA cycle. An additional