Tamara Kiechle | PubMed Health

PubMed2004

Kyphoplasty enhances function and structural alignment in multiple myeloma.

We prospectively evaluated 19 patients with multiple myeloma who had kyphoplasty for vertebral compression fractures. Functional status was assessed preoperatively and 3 months postoperatively using the Oswestry Disability Index. Restoration of anterior and midvertebral height was assessed using lateral radiographs. Meaningful improvement occurred in 16 of 19 patients, with a reduction of the average Oswestry Disability Index from 49 +/- 16.6 to 32.6 +/- 13.6. Partial restoration of anterior vertebral body height was achieved in 76% of levels with an average of 37.8% restoration of the defect. Partial restoration of midvertebral body height was achieved in 91% of levels with an average restoration of 53.4% of the defect. There were no significant complications. These results were compared with results of a cohort of 26 patients with osteoporotic compression fractures treated with kyphoplasty at 37 levels. There was no difference between the groups in terms of Oswestry Disability Index improvement and midvertebral height restoration after 3 months. Greater anterior vertebral height restoration was achieved in the osteoporotic group (51.2% versus 37.8%). Kyphoplasty is a safe treatment modality for myeloma-related vertebral compression fractures. Efficacy in terms of pain relief and functional outcome is comparable with the results in patients with osteoporosis.

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PubMed2002

Cytochrome C and caspase-9 expression in Huntington's disease.

There is increasing evidence implicating apoptosis-mediated cell death in the pathogenesis of neurodegenerative diseases. One important event in the apoptotic cascade is the release of cytochrome c by mitochondria into the cytoplasm, activating caspase-9, leading to the subsequent activation of downstream executioner caspases. In the present study, we examined the distribution of cytochrome c and caspase-9 in Huntington's disease (HD) patients and in a transgenic model of HD (R6/2 line). Neuronal cytochrome c immunoreactivity increased with neuropathological severity in HD patients. Concomitant with this finding, Western-blot analysis showed a shift in the distribution of cytochrome c from the mitochondrial to the cytosolic fraction with incremental cytosolic expression associated with greater striatal degeneration. Active caspase-9 immunoreactivity was present in both HD striatal neurons and in Western blots of severe-grade specimens. Similar findings were observed in the R6/2 mice. There was a temporal increase in expression and shift of cytochrome c from the mitochondrial to the cytosolic fraction from 4-13 wk of age. Activated caspase-9 and caspase 3 activities were present only at endstage disease. Although the present results provide evidence that key components of the intrinsic mitochondrial apoptotic pathway are activated in both HD patients and a transgene murine model of HD, these phenomena are prominent in only severe neuropathological grades in HD patients and HD mice, suggesting that apoptosis may play a greater role in neuronal death at endstage disease.

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