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Biomedical subjects

L Penning

Publications and source records attributed to L Penning.

80 records · Page 5Linked to original sources
PubMedDate not supplied

Biomechanics of lumbosacral dural sac. A study of flexion-extension myelography.

Measurements were performed on 40 lateral lumbar myelograms in flexion and extension with the object of analyzing changes in position and shape of the dural sac in spinal movements. There proved to be an anterior displacement of the entire lumbar dural sac in lumbar extension, most likely caused by shortening and thickening of the flaval ligaments. In addition, the anterior dural surface was indented at the L3-4 and L4-5 interspaces by posterior bulging of the discs in extension. This encroachment was partially compensated by dural bulging into areas with a rich and compressible venous plexus: behind the vertebral bodies and the L5-S1 disc. While the patterns of dural movements showed individual variations, these trends were found in all diagnostic and anatomic subgroups. One subgroup (with root involvement at L4-5) showed marked dorsal encroachment upon the dural sac in extension at the same level. The clinical implications of these findings are discussed.

Biomechanical Phenomena↗
PubMedDate not supplied

Influence of spinal posture on abnormalities demonstrated by lumbar myelography.

During spinal movements the dural end sac undergoes displacement and deformation, chiefly because of bulging of intervertebral disks and flaval ligaments in lumbar extension. Under normal circumstances these dural changes of form do not lead to clinical symptoms. However, in patients with spinal stenosis radiologic signs may be accentuated in lumbar extension. These tend to disappear in flexion. This implies that examination techniques performed in extension (prone lumbar myelography) tend to enhance abnormalities, while techniques in which the spine is more or less flexed (epidural phlebography, computed tomography) tend to mask them. In addition, there may be discrepancy between the picture during surgery (usually in lumbar flexion) and the situation in which a patient experiences symptoms (usually in lumbar extension in spinal stenosis).

Diagnosis, Differential↗
PubMedDate not supplied

TNF-induced intracellular signaling leading to gene induction or to cytotoxicity by necrosis or by apoptosis.

TNF-induced apoptosis, e.g. in murine PC60 cells, requires the TNF receptor p55 (TNF-R55) and the TNF receptor p75 (TNF-R75); the latter even does not have to be triggered. The intracellular domain of TNF-R55 can be activated in the cytosol by linking it to the trimeric CAT protein; induction of this fusion protein leads to a full TNF response. A new MAP kinase, p38, has been shown to be also activated by TNF. This activation is essential for gene induction, but not for cytotoxicity in L929 cells. TNF treatment of L929 leads to reactive oxygen formation in the mitochondria, resulting in cell death by necrosis. TNF treatment of many other cell types results in apoptosis, and this process involves activation of one or more ICE homologs (IHO). In the mouse, seven cysteine proteases of the IHO family have been cloned and partially characterized. One or more of these IHOs is involved in cell killing by proteolysis of critical substrate(s). One substrate, which may be a key effector molecule in the apoptotic process, is PITSLRE kinase.

Animals↗