Search PubMed⌕ Search

Biomedical subjects

Christoph Ulrich

Publications and source records attributed to Christoph Ulrich.

3 recordsLinked to original sources

Intramedullary k-wire fixation of metacarpal fractures.

INTRODUCTION: The majority of metacarpal fractures can be treated conservatively. Nevertheless, surgical treatment is justified in certain cases. Palmar dislocation of >30 degrees and shortening of >5 mm will significantly affect extension and flexion of the hand. Consequently, surgical treatment is indicated. The aim of our study was to evaluate the clinical results of intramedullary Kirschner-wire fixation of metacarpal fractures. MATERIAL AND METHODS: In a retrospective study we analyzed the clinical results of 35 patients with metacarpal fractures that had been treated by closed reduction and elastic fixation with at least two intramedullary k-wires. RESULTS: Most of the patients were young, with good bone quality and low anesthetic risk, and they had suffered the fractures as a result of a direct trauma. Predominantly uncomplicated, the fractures were metaphyseal, subcapital and of the fifth metacarpal bone (750.3-B1 fractures). Surgical treatment was indicated for a palmar axis dislocation of >20 degrees or if a rotatory deficiency was present. Metacarpal joint function and correction of rotatory displacement could be assessed on median after a period of 1.1 year. In 34 patients flexion and extension was normal on both sides. In one patient we found an extension deficiency of 15 degrees and a rotatory deficiency of 10 degrees . In 34 out 35 patients with metacarpal fractures, minimally invasive intramedullary k-wire osteosynthesis resulted in complete restoration. CONCLUSIONS: Intramedullary k-wire fixation is a minimally invasive method for stabilizing metacarpal fractures. The excellent long-term clinical results are due to the fact that the gliding tissue around the fracture will not be affected at all by the surgical procedure.

Adolescent↗

Unreamed tibia nail (UTN) bending: case report and problem solution.

BACKGROUND: An unreamed tibia nail (UTN), implanted for operative stabilization of the tibia after a distal shaft fracture of the lower leg, was bent by excessive load prematurely applied during the healing process, whereby the cross-section-dependent maximum torque permitted in the edge fiber of the UTN during bending load was exceeded. Straightening of the bent, not broken UTN by hand was impossible. Therefore, the bent UTN could only be removed by causing additional damage to the tibia, which is why bending of the nail must be avoided. CONCLUSION: Our analysis shows that modification of the arrangement of the locking holes by 45 degrees increases bending load capacity of the UTN, which can minimize the probability of the occurrence of a bent nail.

Biomechanical Phenomena↗

Expression pattern and regulation of heme oxygenase-1/heat shock protein 32 in human liver cells.

Heme oxygenase-1 (HO-1) is a stress response protein that is highly inducible under various conditions, such as oxidative or heat stress. The present study investigated expression pattern and regulation of HO-1 in human liver. Expression pattern of HO-1 immunoreactive protein was studied in liver biopsies by immunohistochemistry, revealing constitutive expression in Kupffer cells but not in hepatocytes. HO-1 was, however, inducible in hepatocytes and vascular tissue under pathological conditions, e.g. associated with fatty degeneration or liver malignancies. Regulation of HO-1 gene expression was further studied by Northern blot analysis in HepG2 cells and freshly isolated peripheral blood mononuclear cells as model systems of parenchymal and nonparenchymal liver cell populations, respectively. HO-1 mRNA was inducible in HepG2 cells and mononuclear cells by various agents inducing oxidative stress. However, HO-1 gene expression was not inducible by heat shock. Pyrrolidine dithiocarbamate, an inhibitor of nuclear factor kappaB-dependent gene expression, dose dependently decreased HO-1 mRNA transcripts in human mononuclear cells subjected to oxidative stress while slightly increasing HO-1 gene expression in HepG2 cells. In contrast, HO-1 induction upon oxidative stress was attenuated in HepG2 cells by cycloheximide and dexamethasone. Although activator protein-1 has been reported as the predominant redox-sensitive transcription factor inducing HO-1 expression in murine macrophages, nuclear factor kappaB seems to play a significant role in human mononuclear cells. Our data are consistent with a role for activator protein-1 in HO-1 induction in human HepG2 hepatoma cells. These data suggest a differential regulation of HO-1 gene expression in parenchymal and non-parenchymal human liver cells and may provide a topographic basis for the understanding of the role of the heme oxygenase/carbon monoxide pathway in human liver disease.

Blotting, Northern↗