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Forschung 2019
(2019)
Forschungsbericht 2012
(2012)
A low-cost wax-cast molding technique for structuring ultrasoft (Young’s modulus ≤ 40 kPa), agglutinative magnetorheological elastomer (MRE) material is presented. MRE structures ranging from a few millimeters down to the micrometer range with highly reproducible results are possible. Semitransparent MREs are also fabricated and their surfaces modified accordingly. This method opens new possibilities for MREs in biomedical engineering and microfluidic applications. © 2012 Wiley Periodicals, Inc. J. Appl. Polym. Sci., 2013
Optical fiber sensors based on intensity measurement require some form of intensity referencing to avoid errors arising from parasitic losses. Known techniques of referencing such as balanced bridge, divided beam systems or two-wavelength referencing are not suitable for low-cost applications since they use relatively complicated optical components such as multiple LED sources, couplers, filters etc. In this work a novel method of referencing in an extrinsic optical fiber sensor system utilizing temperature dependence of absorption edge in a semiconductor crystal is described. The sensor system comprises a single LED source and no optical fiber junctions. The emission spectrum of an LED depends on its temperature. The reference is provided by controlling the temperature of an LED source and transmission measurements with different emission spectra. The entire process is controlled by a microprocessor unit. Performance of a sensor system is investigated and it is shown that the losses in connectors may be compensated for.
Evaluation of highly compliant magneto-active elastomers with colossal magnetorheological response
(2014)
Highly compliant elastomers with a shear storage modulus as low as 25 Pa are prepared using commercially available silicone, plasticizer, and tactile mutator silicone additive. They are used as matrix material for magneto-active elastomers (MAEs) with carbonyl iron contents between 0 and 85 wt %. In the absence of an external magnetic field, the storage modulus of MAEs based on two selected mixtures ranges between ~100 Pa and ~2000 Pa. Addition of a mutator to the matrix mixture results in a long post-cure period depending on the curing temperature and the initial mixture. In the presence of a magnetic field, the presented MAEs exhibit a strong magneto-induced change in storage modulus resulting in a colossal magnetorheological effect of >106 % which is ~30 times higher than previously reported values. The results are of interest in applications using such elastomers as cell substrates with magnetically tunable rigidity.
Mechanical cues such as extracellular matrix stiffness and movement have a major impact on cell differentiation and function. To replicate these biological features in vitro, soft substrata with tunable elasticity and the possibility for controlled surface translocation are desirable. Here we report on the use of ultra-soft (Young’s modulus <100 kPa) PDMS-based magnetoactive elastomers (MAE) as suitable cell culture substrata. Soft non-viscous PDMS (<18 kPa) is produced using a modified extended crosslinker. MAEs are generated by embedding magnetic microparticles into a soft PDMS matrix. Both substrata yield an elasticity-dependent (14 vs. 100 kPa) modulation of α-smooth muscle actin expression in primary human fibroblasts. To allow for static or dynamic control of MAE material properties, we devise low magnetic field (≈40 mT) stimulation systems compatible with cell-culture environments. Magnetic field-instigated stiffening (14 to 200 kPa) of soft MAE enhances the spreading of primary human fibroblasts and decreases PAX-7 transcription in human mesenchymal stem cells. Pulsatile MAE movements are generated using oscillating magnetic fields and are well tolerated by adherent human fibroblasts. This MAE system provides spatial and temporal control of substratum material characteristics and permits novel designs when used as dynamic cell culture substrata or cell culture-coated actuator in tissue engineering applications or biomedical devices.
Smart materials change their properties with external energy supply. Besides the known ferro-fluids and Magneto Rheological Fluid (MRF) also the Electro Active Polymer (EAP) and Magneto Rheological Elastomer (MRE) belong to these intelligent materials. The latest generation of magnetic elastomers represents a new class of composite materials. This consists of small magnetized particles which are sized in the micron or even nanometer range that in turn is bounded in a highly elastic rubber matrix. These materials are very often called MRE. Only recently, it has managed to develop these materials even further, so that very soft composite materials with a young?s modulus up to 10 kPa are possible. These soft polymers could be named magneto-active polymers. The combination of polymers with magnetic materials show novel and often enhanced properties. A precisely controllable young?s modulus and hardness, giant and non-homogeneous deformation behavior and rapid response to the magnetic field opens up new possibilities for various applications. Since MAP represent a very new technology, the behavior of these materials as a function of their composition and external conditions so far are not yet sufficiently understood. Therefore, some fundamental studies are necessary. In this paper, the mechanical surface properties are studied using a micro hardness meter. This work shows the possibility to control mechanical properties at the surface of MAP with new developed magnetic systems.
Purpose:
Patients with primary open-angle glaucoma (POAG) show a stiffer peripapillary sclera, reactive astrocytes and a remodeled lamina cribrosa (LC). The changes are thought to be mediated by TGFβ2 and its downstream mediator CTGF. Recently we developed a murine glaucoma model by overexpressing CTGF in the anterior eye (βb1CTGF). In this study we investigated the glial lamina region of βb1CTGF mice, and the changes of astrocytes in response to CTGF and TGFβ2 as well as increasing substratum stiffness.
Methods:
Tangential sections of the glial LC of 2-month-old βb1CTGF mice and their wild-type littermates (WT) were stained with phalloidin and antibodies against GFAP, CTGF and fibronectin (FN). Murine optic nerve (ON) astrocytes from CD1 mice were isolated, cultured and characterized by GFAP staining. The astrocytes were treated with TGFβ2 (1ng/ml) and CTGF (50ng/ml and 100ng/ml). In addition, the cells were seeded on PDMS substrata with different stiffness (10, 30 and 60 kPa). Treated cells were analyzed by Western blotting, real-time RT-PCR and immunohistochemistry. Wound healing assays were performed to analyze migration rate following growth factor treatment.
Results:
βb1CTGF mice showed a massive increase in CTGF and GFAP in the glial LC when compared with WT mice. Moreover, an increase in FN staining and phalloidin-labeled actin was observed in the peripapillary sclera. Murine ON astrocytes reacted on increased substrate stiffness by increasing the synthesis of GFAP, vimentin and CTGF. Treatment of the cells with TGFβ2 and CTGF led to an enhanced migration rate. In addition, treatment resulted in an increased expression and synthesis of ECM proteins, including FN, tropoelastin, collagen type I and III. The in vitro findings correlated with those seen in the glaucoma mouse model.
Conclusions:
We conclude that changes in the ECM of LC and peripapillary sclera alter their biomechanical properties and thereby induce reactive changes in resident astrocytes. The reactive changes induced by higher stiffness of their surrounding ECM give rise to a self-amplifying process that includes increased TGFβ2/CTGF signaling and leads to synthesis of ECM and cytoskeletal proteins, a process that in turn augments the stiffness at the optic nerve head (ONH). Such a scenario may finally result in a vicious circle as the causative mechanism for ONH deformation in POAG.
In primary open-angle glaucoma (POAG), a neurodegenerative disease of the optic nerve (ON) and leading cause of blindness, the optic nerve head (ONH) undergoes marked structural extracellular matrix (ECM) changes, which contribute to its permanent deformation and to degeneration of ON axons. The remodeling process of the ECM causes changes in the biomechanical properties of the ONH and the peripapillary sclera, which is accompanied by an increased reactivity of the resident astrocytes. The molecular factors involved in the remodeling process belong to the Transforming growth factor (TGF)-β superfamily, especially TGF-β2. In previous publications we showed that TGF-β2 induced ECM alterations are mediated by Cellular Communication Network Factor (CCN)2/Connective Tissue Growth Factor (CTGF) and recently we showed that CCN2/CTGF is expressed by astrocytes of the ON under normal conditions. In this study we wanted to get a better understanding of the function of CCN2/CTGF under normal and pathologic conditions. To this end, we analyzed the glial lamina and peripapillary sclera of CCN2/CTGF overexpressing mice and studied the effect of CCN2/CTGF and increasing substratum stiffness on murine ON astrocytes in vitro. We observed enhanced astrocyte reactivity in the ONH, increased ECM protein synthesis in the peripapillary sclera and increased Ccn2/Ctgf expression in the ONH during the pathologic development in situ. CCN2/CTGF treatment of primary murine ON astrocytes induced a higher migration rate, and increase of ECM proteins including fibronectin, elastin and collagen type III. Furthermore, the astrocytes responded to stiffer substratum with increased glial fibrillary acidic protein, vimentin, actin and CCN2/CTGF synthesis. Finally, we observed the reinforced appearance of CCN2/CTGF in the lamina cribrosa of glaucomatous patients. We conclude that reactive changes in ONH astrocytes, induced by the altered biomechanical characteristics of the region, give rise to a self-amplifying process that includes increased TGF-β2/CCN2/CTGF signaling and leads to the synthesis of ECM molecules and cytoskeleton proteins, a process that in turn augments the stiffness at the ONH. Such a scenario may finally result in a vicious circle in the pathogenesis of POAG. The transgenic CTGF-overexpressing mouse model might be an optimal model to study the chronic pathological POAG changes in the ONH.