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Only of athletes with no prior concussive history suffered loss of consciousness after an injury compared with of athletes who had suffered three or more concussive episodes.Overall the Glipizide effect in this group was that they were nine times more likely to experience or onfield abnormal signs of injury in a concussive episode.Various theories are discussed to explain these findings.The athletes may have an innate vulnerability to concussion; or the previous episodes may be cumulative.Furthermore other studies cited indicate possible longerlasting cognitive sequelae even years after the event.This is preliminary work with particular flaws in terms of numbers of athletes studied and the possible duration of any cumulative effect.Nonetheless it does raise important questions concerning return to competition in athletes who have suffered repeated relatively minor concussive episodes as well as the more general possible cumulative effects of serial head injuries.In this study two hundred patients who had received levetiracetam were reviewed in a retrospective analysis.Sixteen patients became seizurefree and had improved seizure control.They were compared with the who had deterioration of their seizures.If you are engaged in this kind of research, please stop now.The presence of seizures however was not found to relate to functional outcome at one year.Overall mortality was and was associated with stupor or coma at the start of therapy, older age, and slower cerebral transit estimated from intraarterial angiography.Patients who died also tended to have haemorrhagic infarcts but this probably reflected more extensive thrombosis and was not in itself an adverse risk.One should be vigilant in aggressively managing early symptomatic seizures as they can lead directly to death.The authors raise the question of prophylactic anticonvulsants for patients with haemorrhage but I do not think they have come close to proving the case for so doing.However, phase III clinical studies with vaccine AN had to be halted when some patients developed CNS inflammation. This experimental paper suggests a possible explanation for this outcome.Female CBL mice, weeks old, were immunised with g A. This study illustrates the difficulties of manipulating the immune system for therapeutic purposes.For subscription details please contact the relevant publisher direct.Karger AG Medical and Scientific Publishers,Allschwilerstrasse, CH Basel, SWITZERLAND.Tel, Fax, www.blackwellscience.comepi ACNR VOLUME NUMBER MARCHAPRIL Here we emphasize the use of genetically engineered mouse models that are instrumental for understanding why AD is a neuronal disease, and for validating attractive therapeutic targets.We anticipate that, in the future, therapies based on understanding disease mechanisms will be identified and tested in mouse model systems.The neurodegenerative diseases represent a challenge for science and medicine because of their prevalence, cost, lack of mechanismbased treatments, and impact on individuals and caregivers.They are characterized by dysfunction and death of specific populations of neurons and by the presence, in many instances, of intracellular or extracellular protein aggregates.Although symptomatic treatments are available, there are no mechanismbased treatments.Recent research, particularly in animal models, has begun to provide new insights into the mechanisms of these disorders and has identified new targets for therapy.The identification of mutations in specific genes causing each of these neurodegenerative diseases has provided new Panthenol opportunities to investigate the molecular participants in disease processesand to exp lore pa thogen ic mechanismsusingtr an sgen ic approaches.

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