The allegory of a mountain: an environmental introduction to neurotoxicology.

Overall, the area of human neurotoxicity offers significant difficulties as well as challenges in our attempts to maintain or enhance human well being. Many of the substances to which humans are being exposed are relatively new to the environment, i.e.

Carbon monoxide intoxication: an updated review.

Carbon monoxide (CO), a highly toxic gas produced by incomplete combustion of hydrocarbons, is a relatively common cause of human injury. Human toxicity is often overlooked because CO is tasteless and odorless and its clinical symptoms and signs are non specific. The brain and the heart may be severely affected after CO exposure with carboxyhemoglobin (COHb) levels exceeding 20%.

Carbon monoxide brain toxicity: clinical, magnetic resonance imaging, magnetic resonance spectroscopy, and neuropsychological effects in 9 people.

Carbon monoxide (CO) exposure is a common cause of toxic brain damage, whereby effects range from transient neurological dysfunction to coma and death. A spectrum of severity of magnetic resonance imaging (MRI) findings after CO brain toxicity, including globus pallidus and white matter lesions, is well documented. Reports of MR spectroscopy (MRS) findings re main sparse.

The therapeutic effects of epidural intercellular adhesion molecule-1 monoclonal antibody in a rabbit model: involvement of the intercellular adhesion molecule-1 pathway in spinal cord ischemia.

The pathophysiology of ischemia/reperfusion injury involves extravascular migration of leukocytes from the bloodstream to the site of injury. Leukocyte adhesion and intercellular adhesion molecule-1 (ICAM-1) play an important role in the recruitment of leukocytes to the site of injury. In this study, we evaluated the role of the ICAM-1 in spinal cord ischemia and the therapeutic effects of epidural ICAM-1 monoclonal antibody (Mab).

Acute experimental allergic encephalomyelitis increases lumbar spinal cord incorporation of epidurally administered [(3)H]-D-mannitol and [(14)C]-carboxyl-inulin in rabbits.

Unlabelled: We sought to determine whether acute experimental allergic encephalomyelitis (EAE) alters the incorporation of epidurally administered [(3)H]-D-mannitol and [(14)C]-carboxyl-inulin into the lumbar spinal cord in rabbits. Acute EAE is an experimental model for demyelinating spinal cord diseases such as multiple sclerosis. It was induced in rabbits by footpad inoculation with rabbit spinal cord homogenate, resulting in hind limb paresis or paralysis.