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Temporal thresholds for neocortical infarction in rats subjected to reversible focal cerebral ischemia. Stroke 22: 10321039. Kassel NF, Haley EC Jr, Apperson-Hansen C, and Alves WM 1996 ; Randomized, double blind, vehicle-controlled trial of tirilazad mesylate in patients with aneurysmal subarachnoid hemorrhage: a cooperative study in Europe, Australia, and New Zealand. J Neurosurg 84: 221228. Kawamata T, Katayama Y, Maeda T, Mori T, Aoyama N, Kikuchi T, and Uwahodo Y 1997 ; Antioxidant OPC-14117, attenuates edema formation and behavioral deficits following cortical contusion in rats. Acta Neurochir 70 Suppl ; : 191193. Keli SO, Hertog MG, Feskens EJ, and Kromhout D 1996 ; Dietary flavonoids, antioxidant vitamins, and incidence of stroke: the Zutphen study. Arch Intern Med 156: 637 642. Kilic E, Ozdemir YG, Bolay H, Kelestimur H, and Dalkara T 1999 ; Pinealectomy aggravates and melatonin administration attenuates brain damage in focal ischemia. J Cereb Blood Flow Metab 19: 511516. Knuckey NW, Palm D, Primiano M, Epstein MH, and Johanson CE 1995 ; NAcetylcysteine enhances hippocampal neuronal survival after transient forebrain ischemia in rats. Stroke 26: 305310. Kotake Y 1999 ; Pharmacologic properties of phenyl N-tert-butylnitrone. Antioxid Redox Signal 1: 481 499. Kuroda S, Katsura K, Hillered L, Bates TE, and Siesjo BK 1996 ; Delayed treatment with alpha-phenyl-tert-butyl nitrone PBN ; attenuates secondary mitochondrial dysfunction after focal cerebral ischemia in the rat. Neurobiol Dis 3: 149 157. Larsson A, Orrenius S, Holngren A, and Mannervik B 1983 ; Functions of Glutathione. Biochemical Physiological Toxicological and Clinical Aspects, Raven Press, New York. Lewen A, Matz P, and Chan PH 2000 ; Free radical pathway in CNS injury. J Neurotrauma 17: 871 890. Ling X, Zhang LM, Lu SD, Li XJ, and Sun FY 1999 ; Protective effect of melatonin on injured cerebral neurons is associated with bcl-2 protein over-expression. Zhongguo Yaoli Xuebao 20: 409 414. Love S 1999 ; Oxidative stress in brain ischemia. Brain Pathol 9: 119 131. Maas AI, Steyerberg EW, Murray GD, Bullock R, Baethmann A, Marshall LF, and Teasdale GM 1999 ; Why have recent trials of neuroprotective agents in head injury failed to show convincing efficacy. A pragmatic analysis and theoretical considerations. Neurosurgery 44: 1286 1298. Macdonald RL, Bassiouny M, Johns L, Sajdak M, Marton LS, Weir BK, Hall ED, and Andrus PK 1998 ; U74389G prevents vasospasm after subarachnoid hemorrhage in dogs. Neurosurgery 42: 1339 1346. Manev H, Uz T, Kharlamov A, and Joo JY 1996 ; Increased brain damage after stroke or excitotoxic seizures in melatonin-deficient rats. FASEB J 10: 1546 1551. Marshall LF, Maas AI, Marshall SB, Bricolo A, Fearnside M, Iannotti F, Klauber MR, Lagarrigue J, Lobato R, and Persson L 1998 ; A multicentral on the efficacy of using tirilazad mesylate in cases of head injury. J Neurosurg 89: 519 525. Mattson MP and Camandola S 2001 ; NF B in neuronal plasticity and neurodegenerative disorders. J Clin Invest 107: 247254. McArdle WD, Katch FI, and Katch VL 1999 ; Sports and Exercise Nutrition. Lippincott Williams & Wilkins, Philadelphia. Mcintosh TK, Thomas M, and Smith D 1992 ; The novel 21-aminosteroid U-74006F attenuates cerebral edema and improved survival after brain injury in the rat. J Neurotrauma 9: 33 46. Meister A and Anderson ME 1983 ; Glutathione. Annu Rev Biochem 52: 711760. Memezawa H, Smith ML, and Siesjo BK 1992 ; Penumbral tissues salvaged by reperfusion following middle cerebral artery occlusion in rats. Stroke 23: 552559. Mizui T, Kinouchi H, and Chan PH 1992 ; Depletion of brain glutathione by buthionine sulfoximine enhances cerebral ischemic injury in rats. J Physiol 262: H313H317. Moldeus P, Cotgreune IA, and Berggren M 1986 ; Lung protection by a thiol containing antioxidant N-acetylcysteine. Respiration 50: 531542. Mujika I and Padilla S 1997 ; Creatine supplementation as an ergogenic acid for sports performance in highly trained athletes: a critical review. Int J Sports Med 18: 491 496. Muller A, Cadenas E, Graf P, and Sies H 1984 ; A novel biologically active selenoorganic compound. I. Glutathione peroxidase like activity in vitro and antioxidant capacity of PZ51 Ebselen ; . Biochem Pharmacol 33: 32353239. Nishizawa Y 2001 ; Glutamate release and neuronal damage in ischemia. Life Sci 69: 369 381. Noack H, Kube U, and Augustin W 1994 ; Relations between tocopherol depletion and coenzyme Q during lipid peroxidation in rat liver mitochondria. Free Radic Res 20: 375386. Numagami Y and Ohnishi ST 2001 ; S-Allylcysteine inhibits free radical production, lipid peroxidation, and neuronal damage in rat brain ischemia. J Nutr 131: 1100S 1105S. Ogawa A, Yoshimoto T, Kikuchi H, Sano K, Saito I, Yamaguchi T and Yasuhara H 1999 ; Ebselen in acute middle cerebral artery occlusion: a placebo-controlled double-blind clinical trial. Cerebrovas Dis 9: 112118. Ogawa N, Tsukamoto S, Hirose Y and Kuroda H 1986 ; Survival effect of coenzyme Q10, and naloxone on experimental stroke. Pharmacol Biochem Behav 24: 315317. Oliver CN, Starke-Reed PE, Stadtman ER, Liu GJ, Carney JM, and Floyd RA 1990 ; Oxidative damage to brain proteins, loss of glutamine synthetase activity, and production of free radicals during ischemia reperfusion-induced injury to gerbil brain. Proc Natl Acad Sci USA 87: 5144 5157. O'Neill MJ, Hicks C, Ward M, and Panetta JA 1997 ; Neuroprotective effect of the antioxidant LY231617 and NO synthase inhibitors in global cerebral ischemia. Brain Res 760: 170 178. Packer L 1992 ; New horizons in antioxidant research: action of the thioctic acid dihydrolipoic acid couple in biological systems, in Thioctsaure. 2nd International Thictic Acid Workshop Schmidt K and Ulrich H eds ; pp 35 44, Universimed Verlag GmbH, Frankfurt, Germany. Packer L 1998 ; alpha-Lipoic acid: a metabolic antioxidant which regulates NF!

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Lactic acidosis has received much attention recently as a side effect of certain NARTI drugs, particularly ddI and d4T. This condition is signified by the level of lactic acid in the blood to be 18 mg dl or higher as well as the blood pH to be acidic. Patient fatalities due to excessive enlargement of the liver and acute steatosis are reported in the US and Europe. Initial symptoms vary, and include but are not limited to: substantial increase in liver enzymes, nonspecific gastrointestinal abnormalities, numbness in extremities, weakened muscles, and breathing difficulties. Adis Clinical Trials Insight is a bibliographic and full-text database that contains key papers from more than 1, 700 international medical and biomedical journals on drugs, drug therapy, adverse drug reactions, and pharmacoeconomics. It is divided into five document types: best evidence, citation only, ongoing trial, supporting evidence, and study. Records contain bibliographic and indexing information. Summaries also contain side effects tables, clinical relevance, evaluation scores with positive and negative features, and text, which includes the purpose of the paper, author comments, drug tables listing dosage information, and results tables and amiodarone.

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Protector of Cell Integrity. * Through a variety of actions, including its antioxidant properties, alpha-li0oic acid can help maintain cell integrity in the face of biological threats. Studies * and clinical experiences have shown that alpha-liopic acid can help preserve normal liver function when the body is exposed to certain toxins. * Still other research has found that alphalipoic acid helps protect nerve function by normalizing the transmission of nerve signals in the body. * It also inhibits the activation of "NF B, a genetic transcrip" tion factor that promotes cell destruction and elavil. TABLE 5. Expenditures US$ ; for NISSRP outpatient medicines, according to the benefit coverage level, before and after putting into place the agreement with the pharmaceutical consortium: 1996 real expenditures for January to December ; vs. 1999 nominal expenditures for January to December, for example, alpha lipoic acid topical. From the 1Division of Clinical and Molecular Endocrinology, Case Western Reserve University, Cleveland, Ohio; the 2 Division of Endocrinology, University Hospitals of Cleveland, Cleveland, Ohio; the 3Department of Biostatistics and Epidemiology, George Washington University, Washington, D.C.; and the 4Department of Medicine, Harvard Medical School, Boston, Massachusetts. Address correspondence to Saul Genuth, MD, Room 430, Biomedical Research Building, Case Western Reserve University, 10900 Euclid Ave., Cleveland, OH 44106-4951. E-mail: smg15 cwru . 2005 by the American Diabetes Association and endep. 2007 ADA Scientific Session Oral Presentation Effect of 4-Year Antioxidant Treatment with Alpha-Lipoic Acid in Diabetic Polyneuropathy: The NATHAN 1 Trial Results: The aim of this study was to evaluate the efficacy and safety of [alpha]lipoic acid over 4 years in diabetic patients with mild to moderate distal symmetric polyneuropathy DSP ; . In this multicenter, randomized, double-masked, parallel-group clinical trial 460 diabetic patients with stage 1 or stage 2a DSP were randomly assigned to oral treatment with [alpha]-lipoic acid 600 mg qd ALA; n 233 ; or placebo n 227 ; for 4 years following a 6-week placebo run-in phase. Outcome measures included: Primary outcome measure was a composite score of including the Neuropathy Impairment NIS ; Score of the lower limbs and 7 nerve function tests NIS[LL] + 7 tests; a ; . Secondary outcome measures included the Total Symptom Score TSS nerve symptom change ; , Neuropathy Symptoms and Change NSC ; , NIS, NIS[LL], individual NIS components, motor and sensory nerve conduction attributes, and quantitative sensory testing QST ; . Data analysis was based on the intention to treat. The demographic variables and the outcome measures at baseline were comparable between the groups as were the HbA1c levels during follow-up. The NIS[LL] + 7 tests composite score improved after 4 years vs. baseline by 0.45 [plusmn]0.37 mean[plusmn]SEM ; in the ALA group and worsened by 0.34 [plusmn]0.35 points in the placebo group p 0.105 ; . The NIS and NIS[LL] improved by 0.68 [plusmn]0.44 and 0.34 [plusmn]0.30 points on ALA and worsened by 0.61 [plusmn]0.46 and 0.43 [plusmn]0.31 points on placebo, respectively p 0.028 and p 0.051 ; . The NIS[LL] muscular weakness subscore improved by 0.21[[]plusmn]0.11 on ALA and deteriorated by 0.17 [plusmn]0.15 on placebo p 0.045 ; . The NSC score for weakness severity improved by 0.05 [plusmn]0.03 points on ALA and worsened by 0.04 [plusmn]0.03 points on placebo p 0.008 ; . No significant differences between both groups after 4 years were noted for the nerve conduction parameters and QST. The rates of adverse events were comparable between the groups during the study. In conclusion, 4-year treatment with [alpha]-lipoic acid in mild to moderate DSP is well tolerated and improves some neuropathic deficits and symptoms, but not nerve conduction. Future long-term trials should not anticipate significant progression of DSP in diabetic patients. In assessing patients with headache HA ; , clinicians are often faced with two important questions. Is the HA migraine.? Does the patient require neuroimaging? Patients who present with classic visual aura--a slowly evolving scintillating scotoma that moves or passes through the visual field over roughly 30 minutes, then disappears, and is followed by the onset of unilateral disabling HA--constitute an easy diagnosis. The study suggests 5 questions used as a screening tool for migraine without aura: 1 ; Is the HA pulsating? 2 ; Does it last between 4 and 72 hours without medication ; ? 3 ; Is unilateral? 4 ; Is nausea present? 5 ; Is the HA disabling? If the answer is "yes" to 4 or 5, the likelihood ratio of migraine is high LR 24: migraine vs not-migraine ; . If 3 are present, LR is 3.5. For 1 or 2, the LR is below 1.0 These authors have constructed a mnemonic based on these 5 criteria: POUNDing P PULSATING hO HOURS OF DURATION 4 to72 ; U UNILATERAL N NAUSEA OR VOMITING D DISABLING Looking for a combination of symptoms is important in the diagnosis of migraine and caduet. He touted the development as a sign that the united states had turned the corner in the drug war.

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Two of the most important antioxidant supplements that help protect the heart, the brain, and other tissues are xlpha-lipoic acid and coenzyme Q10. Research continues to expand our knowledge of these two nutrients. While they are not exactly vitamins, as they are manufactured in the body, with stress or aging the need for them increases while the production declines. Aging is accelerated by oxidative stress, DNA deterioration, mitochondrial decline, inflammation, and sugar-protein complexes called advanced glycation endproducts AGE ; , all of which are increased by a number of chronic health conditions, such as diabetes. With the right diet, exercise, and supplements, you can slow down this process and preserve physiological functions for many extra years of vigorous activity. Alphx-lipoic acid ALA ; is a sulfur-containing molecule and a potent antioxidant that is both water and fat soluble It protects against free radicals that are related to both oxygen and nitrogen. As part of the antioxidant network of molecules, it helps to regenerate other antioxidants, such as vitamins C and E. ALA is also a cofactor for enzymatic functions involved in mitochondrial energy production, amino acid metabolism, and production of both DNA and RNA in ways that might reduce chronic inflammation. Some laboratory tests suggest more far-reaching benefits from large amounts of ALA. Oxidative damage to certain enzymes reduces the elasticity of lung tissue, associated with chronic obstructive lung disease. ALA helps to preserve the elastin protein. In the normal course of producing energy, mitochondria create oxygen free radicals that damage the mitochondria if they are not neutralized. This damage from oxidation leads to inefficiency of energy production with age. High doses of ALA can prevent some of this deterioration by mopping up those free radicals. Animal studies support this protective role for ALA. A recent scientific review shows that cancer patients treated with oxaliplatin Eloxatin ; who develop neuropathy a common side effect ; can be effectively treated with supplements of ALA. Earlier researchers used 600 mg of ALA intravenously once a week for 3 to 5 weeks, followed by. DESCRIPTION: Clinical Laboratory Services For Southwest CT Mental Health System Both Urine and Blood Tests Are Required ; FOR: Southwest CT Mental Health System 97 Middle St. Bridgeport, CT 06604 1635 Central Ave., Bridgeport, CT and 780 Summer St., Stamford, CT and chlorthalidone and alpha-lipoic, for instance, alpha lipoic acid and biotin.

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Supplement Facts Serving Size: 1 Capsule Vitamin E as natural d-alpha tocopherol succinate with mixed tocopherols and tocotrienols ; Coenzyme Q-10 L-Carnitine L-Tartrate Alpha-Lipoic acid Tototrienol concentrate Nutriene ; * Daily Value not established. Amount Per Softgel % Daily Value 7.5 IU 25% 5 mg 75 mg 25 mg 5 mg.

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L-carnitine supports the participation of long-chained fatty acids triglycerides ; for the oxidation inside mitochondria. L-carnitine deficits increase glucose metabolism and facilitate a switch to aerobic glycolysis Warburg Phenomenon ; . The disturbance in triglyceride transport causes lipid accumulation, which is often observed in treatment with HAART and protease inhibitors Brinkmann 1999 ; . Pre-AIDS and AIDS have been shown, in the context of a L-carnitine deficit, to be systemic dysfunctions of lipometabolism and of the lipid composition of the T-lymphocytes De Simone 1991 ; . Administrating high doses of Lcarnitine, 6 grams per day for two weeks, has improved T-helper cell proliferation, lowered the triglyceride serum levels and decreased the serum values of circulating beta-2 microglobulins and alpha tumor necrosis factors as indicators for hyperactivation of macrophages in HIV positives and AIDS patients. L-carnitine also appears to stabilize the cytokine balance by ameliorating mitochondrial performance overview with De Simone 1993 ; . Reduced mitochondrial performance as consequence of chemotherapeutics, caused by damage to mitochondrial DNA after the intake of AZT etc. and Bactrim etc., can additionally be compensated by the daily dose of 600 mg lipoic acid alpha-lipoic acid ; plus 300 mg thiamine vitamin B1 ; for a month or longer. Alpha-lipoic acid, a glutathione-elevating agent, increases the LD50 in mice with a dose reduction factor DRF ; of 1.26 [84]. Vitamin E, Vitamin C and b-carotene protected rodents against the acute effects of irradiation [7079]. Vitamin A and b-carotene protected normal tissue during radiation therapy of cancer in an animal model [78]. A combination of vitamin A, C and E protected against radiation-induced myelosuppression during radiation therapy of cancer in an animal model [79]. It has been reported that L-selenomethionine and several different types of antioxidants vitamin C, vitamin E, glutathione, n-acetylcysteine NAC ; , lipoic acid and co-enzyme Q10 and soy bean-derived Bowman-Birk inhibitor ; protected human cells in culture and rats in vivo against oxidative stress produced by photons, protons and 1 GeV iron ions [41].