Cortical devascularization: quantitative diffusion weighted magnetic resonance imaging and histological findings.

This study investigates the development of a small focal cortical lesion produced in a model of brain injury. Two approaches were chosen: diffusion weighted magnetic resonance imaging (DWI) and histology. DW images were collected before devascularization and at 0.5, 1, 2, 3, 5, 7 and 14 days after treatment. Apparent diffusion coefficient (ADC) maps were calculated from the DW images to quantify lesion development. As a second measure of injury, tissue morphology was analyzed using cresyl violet histochemistry. A significant reduction in ADC values within the cortex below the injury site by 0.5 days after surgery was observed. Between 5 and 14 days the ADC values recovered to control levels. ADC changes were also observed in the contralateral cortex at 0.5, 1 and 5 days. The decrease in ADC observed at the early time points suggested cytotoxic edema, whereas the recovery to control levels at later time points suggested infarct formation. This model of brain injury resulted in progressive but relatively slow formation of a pan-necrotic infarct within 14 days. In particular, substantial amounts of cell death were not observed until 2 days after surgery. Overall, the quantitative and histological measures of this lesion are consistent with those observed for an ischemic type of injury, however, the time course of these lesions' development are consistent with other models of traumatic brain injury. Our data demonstrates that DWI is a highly sensitive metric for ischemic-type damage that results from brain injury.

Macrophages: their myelinotrophic or neurotoxic actions depend upon tissue oxidative stress.

There are still questions regarding whether macrophages found in MS lesions are agents of recovery or of destruction. To address this, we examined in aggregate cultures prepared from dissociated embryonic spinal cord tissue, with or without addition of exogenous macrophages, the effect of menadione-induced oxidative stress. Similar to findings of other laboratories, we observed that in the absence of oxidative stress macrophage enrichment promoted myelinogenesis. In macrophage-poor cultures, menadione at 5 microM had very little effect upon the status of the aggregate cultures; however, increasing this to 10 and 20 microM did result in some damage to axons and myelin. By contrast, in macrophage enriched cultures, menadione at a concentration as little as 5 microM caused the complete destruction of the aggregates. We suggest that in neural tissues that have sufficiently high macrophage numbers, oxidative stress results in a positive inflammatory feedback loop that results in massive tissue destruction. We further suggest that what we see in macrophage-enriched aggregates subjected to oxidative stress may represent what happens in the Marburg-type of MS lesion.

Persistent expression of developmental myosin heavy chain isoforms in the tapered ends of adult pigeon pectoralis muscle fibres.

We have shown previously that in addition to the adult myosin heavy chain (MyHC) isoform present throughout the length of each fast-twitch glycolytic muscle fibre within the pectoralis of the mature chicken, the neonatal isoform is retained in the tapered ends of these fibres. This work, however, has been the only published report of this phenomenon. Here, we tested the hypothesis that similar to the chicken, the ends of mature pigeon pectoralis muscle fibres contain developmental MyHC isoform(s). A histological stain was used to visualize endomysium to assist in the analysis of transverse sections of pectoralis muscle from four mature pigeons. Immunocytochemical techniques were used to localize MyHC isoform(s) characteristic of pigeon pectoralis development. We show that within mature pigeon pectoralis, the ends of both fast-twitch glycolytic and fast-twitch oxidative-glycolytic fibre types express MyHC isoform(s) characteristic of their earlier development. Thus, we extend our findings on chicken to another species and an additional muscle fibre type. Retention of developmental MyHC isoform(s) within the tapered ends of mature muscle fibres may be more widespread than is currently appreciated.