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Background: Based on standard computed tomography (CT) and micro-CT scan axis images, our study aims to analyse the incidence of variation of non-fusion ossification centre in the base of the odontoid and its anatomical structure characteristics, to compare ossification centre images and analyse the possible features of the ossification centre that can influence adult odontoid fractures. Materials and methods: Fifty cases were selected for standard cervical CT of the normal axis bone (second cervical) anatomy to calculate the incidence of variation of the non-fusion ossification centre in the base of the odontoid and the indexes of associated anatomical structure. In addition, five dry bone samples with the odontoid were chosen for micro-CT to analyse the clear anatomic structure of the trabecular bone in the ossification centre. Results: Incidence of variation of non-fusion ossification centre in the base of the odontoid was 28%. In the non-ossification group, the mean sagittal diameter of the base of odontoid (SDBO, mm) was 7.64 ± 1.29 mm, the mean transverse diameter of the base of odontoid (TDBO, mm) was 7.14 ± 1.55 mm, and the SDBO:TDBO ratio was 1.1 ± 0.22. In the ossification group, the mean SDBO was 7.7 ± 1.15 mm, the mean TDBO was 7.38 ± 1.32 mm, and the SDBO:TDBO ratio was 1.07 ± 0.21. There was no significant difference in the associated indexes between the ossification and non-ossification groups (p > 0.05). Micro-CT revealed the micro-structure of trabecular bone in the ossification centre and the close relationship between the trabecular bone and the odontoid. One existing non-ossification centre in the base of the odontoid was found in the five odontoid images. The trabecular bone indexes chosen in the target area of the ossification centre were weaker than those in other areas. Conclusions: The variation rate of the non-fusion ossification centre in the base of the odontoid is relatively high and may be an important factor in the aetiology of type II and III odontoid fractures. (Folia Morphol 2020; 79, 1: 141–147)
Post-mitotic neurons are typically terminally differentiated and in a quiescent status. However, in Alzheimer disease (AD), many neurons display ectopic re-expression of cell cycle-related proteins. Cyclin-dependent kinase 11 (CDK11) mRNA produces a 110-kDa protein (CDK11p110) throughout the cell cycle, a 58-kDa protein (CDK11p58) that is specifically translated from an internal ribosome entry site and expressed only in the G2/M phase of the cell cycle, and a 46-kDa protein (CDK11p46) that is considered to be apoptosis specific. CDK11 is required for sister chromatid cohesion and the completion of mitosis. In this study, we found that the expression patterns of CDK11 vary such that cytoplasmic CDK11 is increased in AD cellular processes, compared to a pronounced nuclear expression pattern in most controls. We also investigated the effect of amyloid precursor protein (APP) on CDK11 expression in vitro by using M17 cells overexpressing wild-type APP and APP Swedish mutant phenotype and found increased CDK11 expression compared to empty vector. In addition, amyloid-β25–35 resulted in increased CDK11 in M17 cells. These data suggest that CDK11 may play a vital role in cell cycle re-entry in AD neurons in an APP-dependent manner, thus presenting an intriguing novel function of the APP signaling pathway in AD.
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