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Study Design: Case report. Objective: To present the second case of Brown-Sèquard syndrome (BSS) produced by type III odontoid fracture managed by conservative treatment. Summary Of Background Data: The occurrence of BSS due to odontoid fracture is scarce. So far 6 cases have been reported, and only 1 is produced by type III odontoid fracture. The possible pathophysiology, clinical course and treatment outcome have been rarely discussed. Methods: A 39-year-old man presented with weakness of his left arm and leg, mild neck pain, and impaired proprioceptive and light touch sensations below the left C2 dermatome. There were decreased pain and temperature sensations below the right C4 dermatome too. Computerized tomography showed odontoid type III fracture with posterior displacement at that level. Magnetic resonance imaging presented focal hyperintensity around the C2 vertebral level. High dose of prednisolone, close reduction with Gardner-Wells tong skull traction, following external stabilization by Halo-Vest and rehabilitation therapy were applied. Results: Complete resolution of neck pain and significant improvement of motor and sensory functions, i.e., light touch and proprioception, were shown 2 months after spinal injury. Impaired temperature discrimination persisted, however. Conclusion: BSS is rarely caused by type III odontoid fracture and this is the second report. Conservative intervention is advantageous for both type III odontoid fracture and BSS which is consistent with previous results. [ABSTRACT FROM AUTHOR]

Somatic mutations in mitochondrial DNA (mtDNA) have been detected in hepatocellular carcinoma (HCC). However, it remains unclear whether mtDNA copy number and mitochondrial biogenesis are altered in HCC. In this study, we found that mtDNA copy number and the content of mitochondrial respiratory proteins were reduced in HCCs as compared with the corresponding non-tumorous livers. MtDNA copy number was significantly reduced in female HCC but not in male HCC. Expression of the peroxisome proliferator-activated receptor ? coactivator-1 was significantly repressed in HCCs (P<0.005), while the expression of the mitochondrial single-strand DNA-binding protein was upregulated, indicating that the regulation of mitochondria biogenesis is disturbed in HCC. Moreover, 22% of HCCs carried a somatic mutation in the mtDNA D-loop region. The non-tumorous liver of the HCC patients with a long-term alcohol-drinking history contained reduced mtDNA copy number (P<0.05) and higher level of the 4977?bp-deleted mtDNA (P<0.05) as compared with non-alcohol patients. Our results suggest that reduced mtDNA copy number, impaired mitochondrial biogenesis and somatic mutations in mtDNA are important events during carcinogenesis of HCC, and the differential alterations in mtDNA of male and female HCC may contribute to the differences in the clinical manifestation between female and male HCC patients.British Journal of Cancer (2004) 90, 2390-2396. doi:10.1038/sj.bjc.6601838 www.bjcancer.com Published online 4 May 2004 [ABSTRACT FROM AUTHOR]