Nervous system injury

Tso and Lam suggested that astaxanthin could be useful for prevention and treatment of neuronal damage associated with age-related macular degeneration and may also be effective in treating ischemic reperfusion injury, Alzheimer s disease, Parkinson s disease, spinal cord injuries, and other types of central nervous system injuries. Astaxanthin was found to easily cross the blood-brain barrier and did not form crystals in the eye. 

Glasgow Coma Scale (GCS) A scale for evaluating level of consciousness after central nervous system injury (evaluates eye opening and verbal and motor responsiveness). 

Neurotrophic factors promote both cell survival and axon growth after adult central nervous system injury in-vivo 524... 

CENTRAL NERVOUS SYSTEM INJURY AND COMPENSATORY PLASTICITY 524... 

David, S. and Aguayo, A. J. Axonal elongation into peripheral nervous system bridges after central nervous system injury in adult rats. Science 214 931-933,1981. 

Chopp, M., Chan, P. H., Hsu, C. Y., Cheung, M. E. and Jacobs, T. P. DNA damage and repair in central nervous system injury National Institute of Neurological Disorders and Stroke Workshop Summary. Stroke 27 363-369,1996. 

Most cases of mercury poisoning led to handicap, chronic disease, or death. The most frequent symptoms include numbness of limbs, lips and tongue, speech abnormalities, limb function disorders, visual acuity disorders, deafness, and muscular atrophy. Insomnia, hyperactivity, and coma have also been reported. Methylmercury penetrates the blood-brain barrier and causes central nervous system injuries. Mercury also has a teratogenic effect, leading to congenital abnormalities or congenital Minamata disease. 

Loss of enzyme activity, autoantigenicity DNA damage, nucleoprotein clumping, autoantigens Brain and peripheral nervous system injury Chronic inflammation, fibrosis, granulomas, interference in clearance of infectious agents ... 

Pharmacological issues (i) Renal handhng of magnesium . (ii) Metabolic effects of diuretics , (iii) Myocardial infraction , (iv) Hypomagnesemia, (v) Central nervous system injury . 

Correale J. and Villa A. (2004). The neuroprotective role of inflammation in nervous system injuries. J. Neurol. 251 1304-1316. 

Gilgun-Sherki Y., Rosenbaum Z., Melamed E., and Offen D. (2002). Antioxidant therapy in acute central nervous system injury Current state. Pharmacol. Rev. 54 271-284. 

Allan S. M. and Rothwell N. J. (2003). Inflammation in central nervous system injury. Philos. Trans. R. Soc. Lond B Biol. Sci. 358 1669-1677. 

Central nervous system injury is a common effect associated with exposure to vapors of chlorobenzene in humans. Studies in animals suggest that chlorobenzene can also result in damage to the liver and kidneys. Since similar effects occur with exposure to other chemicals, additional studies are needed to identify more specific biomarkers by which to monitor populations living near hazardous waste sites. 

Today, with the exception of bone marrow for hematopoietic reconstitution, therapeutic cellular transplantation is an emerging technology. In recent years novel approaches in the potential restoration of function through cellular transplantation have included the use of fetal human or xenogeneic neural tissue for Parkinson s disease, ectopically implanted pancreatic islets for diabetes, Schwann cells and olfactory ensheathing glia for spinal cord injury, encapsulated chromaffin cells for pain, and various types of stem cells for the treatment of diabetes, cardiac disease, and central nervous system injuries or disease [2], There have also been trials of encapsulated cells to provide enzymes that either remove toxic products or provide activation of prodrugs to therapeutics, usually anticancer derivatives. 

Free radicals in central nervous system injury... 

Karmel BZ, Gardner JM, Freedland RL. Arousal-modulated attention at four months as a function of intrauterine cocaine exposure and central nervous system injury. J Pediatr Psychol 1996 21(6) 821-32. 

Lithium Toxicity. Lithium toxicity is a life-threatening complication. The blood levels required for a therapeutic effect are very close to those leading to toxicity. Typically, doses of lithium are aimed at reaching blood levels of 0.6-1.2 mEq/L. Early signs of toxicity may appear at levels above 1.5 mEq/L and become quite serious above 2.0 mEq/L. If not recognized and treated on a timely basis, lithium toxicity can lead to serious central nervous system injury and even death. The elderly are particularly sensitive to even therapeutic levels of lithium, and their levels tend to fluctuate more unpredictably, thus requiring closer monitoring. 

SAFETY PROFILE Moderately toxic by ingestion and skin contact. A skin and eye irritant. Experimental teratogenic effects. Other experimental reproductive effects. Causes severe central nervous system injury to experimental animals. Mutation data reported. Combustible when exposed to heat or flame can react with oxidizing materials. To fight fire, use CO2, dry chemical. When heated to decomposition it emits acrid smoke and irritating fumes. 

It is moderately irritating, particularly to the eyes. While information on the systemic toxicity of this specific tin compound is lacking, it should be assumed that cyhexatin can be absorbed to some extent across the skin and that substantial absorbed doses would cause nervous system injury... 

Schwai tz M (2003) Macrophages and microglia in centi al nervous system injury Ai e tliey helpful or haiTnful J Cereb Blood Flow Metab 23 385-394. 

Franzen R, Bouhy D, Schoenen J (2004) Nervous system injury Focus on the inflammatory cytokine granulocyte-macrophage colony stimulating factor . Neurosci Lett 361 76-78. 

Meisel C, Schwab JM, Brass K, Meisel A, Dimagl U (2005) Central nervous system injury-induced immune deficiency syndrome. Nat Rev Neurosci 6 775-786. 

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