Underwater 3D Surface Measurement Using Fringe Projection Based Scanning Devices.

In this work we show the principle of optical 3D surface measurements based on the fringe projection technique for underwater applications. The challenges of underwater use of this technique are shown and discussed in comparison with the classical application. We describe an extended camera model which takes refraction effects into account as well as a proposal of an effective, low-effort calibration procedure for underwater optical stereo scanners. This calibration technique combines a classical air calibration based on the pinhole model with ray-based modeling and requires only a few underwater recordings of an object of known length and a planar surface. We demonstrate a new underwater 3D scanning device based on the fringe projection technique. It has a weight of about 10 kg and the maximal water depth for application of the scanner is 40 m. It covers an underwater measurement volume of 250 mm × 200 mm × 120 mm. The surface of the measurement objects is captured with a lateral resolution of 150 µm in a third of a second. Calibration evaluation results are presented and examples of first underwater measurements are given.

Investigating the functional role of CD2BP2 in T cells.

The adaptor protein CD2-binding protein 2 (CD2BP2) confers binding to proline-rich sequences (PRS) via its GYF domain. In addition to the cytoplasmic domain of CD2, several other proteins were identified as interaction partners of CD2BP2, but the in vivo significance of these findings is unclear. We now show that CD2BP2's nuclear localization is not changed when CD2 and CD2BP2 are co-expressed in HeLa cells, indicating that other PRS compete effectively for CD2BP2 binding in the nucleus. Since the CD2BP2-binding motifs of CD2 are known to be involved in cytokine signaling, we tested the effect of CD2BP2 knockdown in PBMCs on the expression of T-cell cytokines. No major difference in cytokine expression can be observed for primary cells transfected with CD2BP2-specific small interfering RNA. We conclude that CD2 signaling is at least partially independent of its in vitro binding partner CD2BP2.

Cysteine-scanning mutagenesis of transmembrane segment 1 of glucose transporter GLUT1: extracellular accessibility of helix positions.

Transmembrane segment 1 of the cysteine-less GLUT1 glucose transporter was subjected to cysteine-scanning mutagenesis. The majority of single-cysteine mutants were functional transporters, as assessed by 2-deoxy-d-glucose uptake or 3-O-methyl-d-glucose transport. Substitution of cysteine for Leu-21, Gly-22, Ser-23, Gln-25, and Gly-27, however, led to uptake rates that were less than 10% of that of the nonmutated cysteine-less GLUT1. NEM, a membrane-permeable agent, was used to identify positions that are sensitive to transport alteration by sulfhydryl reagents, whereas uptake modification by the membrane-impermeant pCMBS indicated accessibility to water-soluble solutes from the external cell environment. Twelve of the 21 single-cysteine mutants were significantly (p < 0.01) affected by NEM, and on the basis of this sensitivity, four positions were identified by pCMBS to form a water-accessible surface within helix 1. The pCMBS-sensitive positions are localized at the exofacial C-terminal end along a circumference of the helix.

Optical modeling of extraoral defects.

In order to reduce the stress caused to patients by conventional methods of modeling using computed tomography (CT) or magnetic resonance imaging (MRI), an optical modeling process has been developed for extraoral defects and body areas. The selected body part is digitized using optical 3-coordinate measuring technology, providing an extensive data record. This is adapted for further use by equalizing the point clouds to obtain a Computer Aided Design (CAD) model, which is converted to a physical model by means of a stereolithographic process. With this technology, the patient's physical and psychological stress may be reduced. This article describes a technique for optical modeling of an ocular prosthesis.

Bone marrow-derived cells expressing green fluorescent protein under the control of the glial fibrillary acidic protein promoter do not differentiate into astrocytes in vitro and in vivo.

Differentiation of bone marrow (BM) cells into astroglia expressing the glial fibrillary acidic protein (GFAP) has been reported in vitro and after intracerebral or systemic BM transplantation. In contrast, recent data suggest that astrocytic differentiation does not occur from BM-derived cells in vivo. Using transgenic mice that express the enhanced green fluorescent protein (GFP) under the control of the human glial fibrillary acidic protein (GFAP) promoter, we investigated the potential of adult murine BM-derived cells to differentiate into macroglia. In the brains of GFAP-GFP transgenic mice, astrocytes were brightly fluorescent from the expression of GFP. When BM from these animals was transplanted into lethally irradiated wild-type animals, the transgene was detected in the reconstituted hematopoietic system, but no GFP expression was found in the nervous system. In contrast, GFAP-GFP neuroectodermal anlage grafted into adult wild-type striatum gave rise to GFP-expressing astrocytes. Because cerebral ischemia has been suggested to promote the differentiation of BM-derived cells into astrocytes, BM chimeric mice were subjected to focal cerebral ischemia. No GFP-positive cells were found in the ischemic or contralateral hemispheres of these brains. Even after direct injection of GFAP-GFP transgenic BM cells into wild-type striatum, no GFP-expressing astroglia were detected. To test the hypothesis that the in vitro environment might be more permissible for astroglial differentiation, we cultured BM from mice that constitutively express GFP, BM cells expressing GFP from a retroviral vector, and BM from GFAP-GFP transgenic mice on astrocytes and on organotypic hippocampal slices. In all experimental paradigms, BM-derived cells were found to differentiate into ramified microglia but not into GFAP-expressing astrocytes.