Changes in the activity of blood serum enzymes in acute intoxication with hypnotic and sedative drugs.
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Biomedical subjects
Publications and source records attributed to J Hanke.
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The staging method proposed by Braak and Braak allows the objective and reliable assessment of Alzheimer-related neurofibrillary pathology. Originally the method was designed for 100-microm thick sections. However, the use of thick sections proved to present difficulties in a routine neuropathology laboratory. In order to adapt the staging method for thin paraffin-embedded sections, we performed an inter- and intrarater study analysing the reliability of the staging method in thin sections. Statistical analysis of the data provided by six independent examiners in two rating sessions reveal kappa values of 0.6-0.8 for both the interrater and the intrarater reliability. The average rate of mistake of the examiners was rarely bigger than a half stage. We conclude that the adapted staging method in thin sections is strongly reliable and we recommend it for staging purposes in institutions where the preparation of thick sections would be difficult.
Extracellular deposits of the beta-amyloid protein and intraneuronal neurofibrillary changes are hallmarks of Alzheimer's disease. Neurofibrillary changes in the cell body of neurons are the neurofibrillary tangles, while beta-amyloid deposits containing dystrophic neurites with neurofibrillary changes are called neuritic plaques. beta-Amyloid deposits and neurofibrillary tangles display a sequential accumulation in the cerebral cortex. In the present study, the topographical distribution of beta-amyloid deposits and neuritic plaques in the entorhinal region, perirhinal cortex and hippocampal formation was investigated in relationship to the amyloid and neurofibrillary staging proposed by Braak. The number of subregions displaying beta-amyloid deposits and neuritic plaques continuously increases in correlation with the amyloid stage (for beta-amyloid deposits r = 0.90, p < 0.0001, for neuritic plaques r = 0.74, p < 0.0001) and neurofibrillary stage (for beta-amyloid deposits r = 0.53, p < 0.0001, for neuritic plaques r = 0.68, p < 0. 0001). Parallel to the advancement in the neurofibrillary stage, early and late predilection sites of beta-amyloid deposits and neuritic plaques can be distinguished. The early predilection sites correspond to projection areas of regions which exhibit incipient neurofibrillary tangles. Furthermore, neuritic plaques only occur in the presence of neurofibrillary tangles in the areas investigated. The findings indicate that neuritic plaques gradually develop in the projection areas of tangle-bearing neurons.
Complex traits are generally taken to be under the influence of multiple genes, which may interact with each other to confer susceptibility to disease. Statistical methods in current use for localizing such genes essentially work under single-gene models, either implicitly or explicitly. In genomic screens for complex disease genes, some of the marker loci must be in tight linkage with disease susceptibility genes. We developed a general multi-locus approach to identify sets of such marker loci. Our approach focuses on affected sib pair data and employs a nonparametric pattern recognition technique using artificial neural networks. This technique analyzes all markers simultaneously in order to detect patterns of locus interactions. When applied to previously published sib pair data on type I diabetes, our approach finds the same genes as in the published report in addition to some new loci. For a specific two-locus model of inheritance, the power of our approach is higher than that of the currently used analysis standard.
The staging method proposed by Braak and Braak is based on the sequential accumulation of neurofibrillary pathology in the cerebral cortex. Unlike the currently used diagnostic criteria for Alzheimer's disease (AD) it does not take into consideration the age of the patients and whether they were demented or not for the establishment of the pathological stage of the disease. To examine the interobserver reliability of the method we performed an inter- and intrarater study using the Braak staging method in 41 brains. The agreement between the examiners and between the diagnoses of the same examiner at different times was almost perfect, the kappa statistics reaching values above 0.90. These findings indicate that the staging, relying on the differential distribution of neuritic pathology in the brain in AD, is a reliable and reproducible method for the description of AD-related pathology. This makes it suitable for brain-banking and research purposes.
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Autograft and allograft bone transplantation is frequently performed to achieve sufficient stability in the primary or secondary treatment of fractures with cortical defects. The ingrowth of bone in his new environment develops in three consecutive periods: the revascularisation, the osteogenic regeneration and the functional adaptation. There is an important histomorphologic difference between the autografts and allografts in the first period of their development. Therefore there are different indications for the performance of autograft or allograft bone transplantation. An autograft bone transplantation implies an adjuvant surgical procedure with possible complications, otherwise after allograft bone transplantation a higher infection risk exists. At the University Clinic of Essen we performed 374 autograft bone transplantations with a complication rate of 2.7% at the donor site and only 0.6% at the receptor site. Infection rate after allograft bone transplantation was 5.7%.
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The entorhinal region is located in the ventromedial surface of the temporal lobe on the parahippocampal gyrus. Occurrence of early argyrophilic neurofibrillary tangles was investigated in brain sections of the left and right entorhinal region of 9 individuals of both sexes between the age of 26 to 54 years. Parasagittal serial sections at 100 microns were performed to include the very anterior part of the entorhinal region. An advanced silver method was used for staining neurofibrillary changes. The neurofibrillary tangles were counted via light microscopy, marked on the sections and staged as proposed by Braak and Braak. In 1 case we found a left-right difference by 1 stage (right: stage I, left: stage II). The tangle distribution in another case exhibited several neurofibrillary tangles only in the very anterior part of the entorhinal cortex on both sides (stage 0). In 3 cases some neurofibrillary tangles occurred in the very anterior part of the right entorhinal region, while a few are present in more posterior parts (stage I). The corresponding left hemisphere showed the same anterior-posterior distribution pattern as on the right in only 1 of these cases. In the remaining 4 cases, no neurofibrillary changes were visible. In conclusion, the very anterior part of the entorhinal region is among the earliest sites for development of neurofibrillary tangles. Distribution of early Alzheimer-related neurofibrillary changes in the entorhinal region displays variabilities in the anterior-posterior direction as well as in a left-right comparison.