Mn (III) tetrakis (4-benzoic acid) porphyrin protects against neuronal and glial oxidative stress and death after spinal cord injury.

This study explores the ability of a catalytic antioxidant, Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP), to protect against neuronal and glial oxidative stress and death after spinal cord injury (SCI). Nine different doses of MnTBAP were administered into the intrathecal space of the rat spinal cord immediately following moderate SCI to establish dose - response curves for prevention of lipid peroxidation and neuron death. An optimal dose was determined by comparing the effectiveness of MnTBAP protection among doses. The optimal dose was then administered and the cords were removed 24 h post-administration and processed for staining. The cells in the cord sections at different distances from the epicenter were counted to obtain the spatial profiles of MnTBAP protection. Comparison of the counts between MnTBAP- and vehicle-treated groups in the sections double immuno-fluorescence-stained with oxidative and cellular markers demonstrated that MnTBAP significantly reduced numbers of nitrotyrosine- and DNP-positive (stained with an antibody against 2,4-dinitrophenyl hydrazine (DNPH)-labeled protein carbonyls) neurons, astrocytes, and oligodendrocytes. Comparison of the counts between the two treatments in the sections immuno-stained with cellular markers revealed that MnTBAP significantly increased numbers of neurons, motoneurons, astrocytes, and oligodendrocytes. MnTBAP more effectively reduced neuronal than glial cell death. Post-injury treatment with the optimal dose of MnTBAP at 6, 12, 24, 48, and 72 h post-SCI demonstrated that the effective time window for reducing protein nitration and neuron death was at least 12 h. Our results demonstrated that MnTBAP combats oxidative stress, thereby attenuating all types of cell death after SCI.

Mn (III) tetrakis (4-benzoic acid) porphyrin administered into the intrathecal space reduces oxidative damage and neuron death after spinal cord injury: a comparison with methylprednisolone.

The metalloporphyrin Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP) is a cell-permeable superoxide dismutase mimetic and a broad-spectrum scavenger of reactive species. Since MnTBAP may not cross the blood-brain barrier, this study evaluated the therapeutic potential of MnTBAP to treat spinal cord injury (SCI; 25 g x cm) by directly administering it into the intrathecal space of the rat spinal cord. The cells in spinal sections removed at 24 h post-SCI were immunohistochemically stained with anti-4-hydroxynonenal (HNE), a marker of membrane lipid peroxidation (MLP); anti-nitrotyrosine (Ntyr), a marker of protein nitration; and anti-neuron-specific enolase (NSE) antibodies. Immunostained neurons were counted for quantitative evaluation. Pre-treatment 30 min before SCI with 1 mg/kg MnTBAP or 4-h post-SCI treatment with 2.5 mg/kg MnTBAP administered into the intrathecal space significantly reduced MLP and protein nitration, and increased the number of surviving neurons compared to vehicle controls. However, post-SCI treatment with a standard regimen of methylprednisolone sodium succinate (MPSS; 30 mg/kg followed by 5.4 mg/kg for maintenance, iv administration), the only drug used for clinical treatment of SCI, not only did not reduce MLP and neuron loss, it increased protein nitration compared with vehicle controls (two-way analysis of variance [ANOVA] followed by the Tukey test). These results demonstrate that pre- and post-intrathecal treatments with the low doses of MnTBAP provide sustained neuroprotection by preventing oxidative stress and that post-treatment with MnTBAP is superior to post-treatment with MPSS in preventing oxidative stress and resulting neuron loss.

An abbreviated history of the ear: from Renaissance to present.

In this article we discuss important discoveries in relation to the anatomy and physiology of the ear from Renaissance to present. Before the Renaissance, there was a paucity of knowledge of the anatomy of the ear, because of the relative inaccessibility of the temporal bone and the general perception that human dissections should not be conducted. It was not until the sixteenth century that the middle ear was described with detail. Further progress would be made between the sixteenth and eighteenth century in describing the inner ear. In the nineteenth century, technological advancement permitted a description of the cells and structures that constitute the cochlea. Von Helmholtz made further progress in hearing physiology when he postulated his resonance theory and later von Békésy when he observed a traveling wave in human cadavers within the cochlea. Brownell later made a major advance when he discovered that the ear has a mechanism for sound amplification, via outer hair cell electromotility.

[Transmissible spongiform encephalopathies]. / Encefalopatías espongiformes transmisibles.

Transmissible spongiform encephalopathies (TSE) are a group of diseases which have received a lot of attention in recent years. The interest on these diseases has been stimulated by the appearance of bovine spongiform encephalopathy (BSE) and the new variant of Creutzfeldt-Jakob disease (nvCJD); the latter is likely to be acquired by ingesting contaminated beef. Until now 109 cases of nvCJD have been reported, most of them occurring in the United Kingdom. Some experts think that this is the beginning of a nvCJD pandemic. Deep knowledge of the mechanisms of transmission of TSE is needed to prevent the emergence of a TSE pandemic in humans. We address various aspects of TSE and discuss prevention methods of TSE in ruminants and humans.

Encefalopatías espongiformes transmisibles / Transmissible spongiform encephalopathies

Transmissible spongiform encephalopathies (TSE) are a group of diseases which have received a lot of attention in recent years. The interest on these diseases has been stimulated by the appearance of bovine spongiform encephalopathy (BSE) and the new variant of Creutzfeldt-Jakob disease (nvCJD); the latter is likely to be acquired by ingesting contaminated beef. Until now 109 cases of nvCJD have been reported, most of them occurring in the United Kingdom. Some experts think that this is the beginning of a nvCJD pandemic. Deep knowledge of the mechanisms of transmission of TSE is needed to prevent the emergence of a TSE pandemic in humans. We address various aspects of TSE and discuss prevention methods of TSE in ruminants and humans.