The keratin intermediate filament cytoskeleton protects epithelial cells against various types of stress and is involved in fundamental cellular processes such as signaling, differentiation and organelle trafficking. These functions rely on the cell type-specific arrangement and plasticity of the keratin system. It has been suggested that these properties are regulated by a complex cycle of assembly and disassembly. The exact mechanisms responsible for the underlying molecular processes, however, have not been clarified. Accumulating evidence implicates the cytolinker plectin in various aspects of the keratin cycle, i.e., by acting as a stabilizing anchor at hemidesmosomal adhesion sites and the nucleus, by affecting keratin bundling and branching and by linkage of keratins to actin filament and microtubule dynamics. In the present study we tested these hypotheses. To this end, plectin was downregulated by shRNA in vulvar carcinoma-derived A431 cells. As expected, integrin β4- and BPAG-1-positive hemidesmosomal structures were strongly reduced and cytosolic actin stress fibers were increased. In addition, integrins α3 and β1 were reduced. The experiments furthermore showed that loss of plectin led to a reduction in keratin filament branch length but did not alter overall mechanical properties as assessed by indentation analyses using atomic force microscopy and by displacement analyses of cytoplasmic superparamagnetic beads using magnetic tweezers. An increase in keratin movement was observed in plectin-depleted cells as was the case in control cells lacking hemidesmosome-like structures. Yet, keratin turnover was not significantly affected. We conclude that plectin alone is not needed for keratin assembly and disassembly and that other mechanisms exist to guarantee proper keratin cycling under steady state conditions in cultured single cells.
The presented mathematical model was capable of quantitatively reconstructing data obtained from different studies of electrophysiology and force development in normal and failing myocardium of humans. In future work, the model can serve as a component for studying macroscopic mechanisms of excitation propagation, metabolism, and electromechanics in human myocardium.
Pleuramesothelioma is a malignant tumor. A computer-assisted diagnosis system shall provide physicians with the assessment of the detected pleural thickening from the 3D CT data. This paper describes a new, improved method to assess the size of detected thickening using both the 2D and 3D thin plate spline. First, a coordinate transformation was applied. Next, set of landmarks was selected as input for the thin plate spline. The final step is the numerical area integration. The results show that the calculated area was more accurate than the former pixel counting technique, and promise further automatic development.
KEY WORDSThin plate spline interpolation, 3D modeling, pleural thickenings, pleural mesothelioma, 3D CT data
Registration of an image non-rigidly to another one causes deformations, which generally do not preserve the initial volume. Volume preservation is however indispensable for observing tumors in medical images. This paper presents the correction of B-spline based registration to preserve the volume in observed regions. In contrast to other approaches, our solution is not obtained through energy minimization, but by calculating the correction parameters for the deformation directly. Especially for high resolution image data this strategy is very efficient in terms of computational expenses. We derive a closed form solution to optimize the registration with respect to the compression at a single point and then extend the problem to multiple points. Finally we prove also that the correction terms do not have any significant influence on the registration quality.
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