Three-dimensional recording of the human face with a 3D laser scanner.

Three-dimensional recording of the surface of the human body or of certain anatomical areas has gained an ever increasing importance in recent years. When recording living surfaces, such as the human face, not only has a varying degree of surface complexity to be accounted for, but also a variety of other factors, such as motion artefacts. It is of importance to establish standards for the recording procedure, which will optimise results and allow for better comparison and validation. In the study presented here, the faces of five male test persons were scanned in different experimental settings using non-contact 3D digitisers, type Minolta Vivid 910). Among others, the influence of the number of scanners used, the angle of recording, the head position of the test person, the impact of the examiner and of examination time on accuracy and precision of the virtual face models generated from the scanner data with specialised software were investigated. Computed data derived from the virtual models were compared to corresponding reference measurements carried out manually between defined landmarks on the test persons' faces. We describe experimental conditions that were of benefit in optimising the quality of scanner recording and the reliability of three-dimensional surface imaging. However, almost 50% of distances between landmarks derived from the virtual models deviated more than 2mm from the reference of manual measurements on the volunteers' faces.     

Influence of triethyl lead on neurofilaments in vivo and in vitro

The influence of triethyl lead chloride (TriEL) on the organization of neurofilaments in vivo was studied by indirect immunofluorescence microscopy employing mouse neuroblastoma cells (Neuro-2a). TriEL induces perinuclear coil formation of neurofilaments in those cells. The rearrangements observed are not correlated with significant changes of the microtubular system. Cells in which the microtubular network was stabilized by Taxol treatment prior to incubation with TriEL even show the rearrangement of the neurofilaments. The effect of TriEL is reversible. In vitro, the effect of TriEL on isolated neurofilaments and on filament formation as well as on the structure of preformed filaments was investigated by electron microscopy. If isolated neurofilaments from porcine spinal cord are incubated in the presence of TriEL, they show constrictions and bulges. Additionally, many fragments are seen. If preformed filaments are treated with TriEL, unraveling of fibers into protofilamentous strands is observed. The assembly of neurofilaments in vitro is disturbed in the presence of TriEL. The interaction of TriEL with neurofilaments in vivo is likely to be at least partly responsible for the neurotoxicity of TriEL.     

5-Oxo-1H-3,4,5,6-tetrahydro-2,6-methano-2-benzazocin und seine Reduktionsprodukte

3,4,5,6-Tetrahydro-1H-2,6-methano-2-benzazocin-5-one and its Reduction Products 3,4,5,6-Tetrahydro-1H-2,6-methano-2-benzazocin-5-one 2 has been prepared by oxidation of N-benzyl-4-piperidone 1 with cerium(IV) sulfate. 2 was reduced by sodium borohydride or lithium aluminum hydride in various solvents. The stereoselectivity of these reductions is high. The configurations of the epimeric alcohols were determined by ¹H-NMR spectroscopy.     

Cerebrospinal fluidCHOLINESTERASES—MARKERS for loss ofcholinergic basal forebrain neurons?

The present study was conducted to test the hypothesis that cholinergic basalforebrain neurons are a major source of cerebrospinal fluid (CSF) cholinesterases. To address thisquestion enzyme activities of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) inboth CSF and parietal cortex were assayed following selective lesion of basal forebrain cholinergicneurons by a single intracerebroventricular application of the cholinergic immunotoxin192IgG-saporin. Cholinergic immunolesions led to a dramatic decrease in total AChE activity inparietal cortex, which was due to the specific loss of the G4 molecular form while the activity ofthe G1 form was increased as compared to nonlesioned animals. In contrast, the total enzymeactivity of BChE and its molecular forms were not affected by cholinergic lesion in both parietalcortex and CSF. The data suggest, that cholinergic basal forebrain neurons are seemingly not amajor source of cholinesterases in the CSF, and do not provide any evidence for using CSFcholinesterases as a diagnostic marker of basal forebrain cholinergic cell loss in humans.     

Medikamentöse Schmerztherapie—ein großes Repertoire an Möglichkeiten

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