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11.
老年性痴呆症患者海马老年斑三维重构 总被引:3,自引:0,他引:3
老年斑是老年性痴呆 (AD)的主要病理特征之一。β 淀粉样蛋白 (Aβ)在老年斑中的积聚与AD发病关系密切。因此 ,如何抑制老年斑内Aβ的积聚和促进Aβ纤维的解聚对于治疗和预防AD有十分重要的意义。通过免疫组织化学染色、MATLAB软件图像处理、AVS重构等技术构建了老年斑三维结构。实验发现海马部位的弥散斑和经典斑具有孔状结构 ;弥散斑无明显核心结构 ,密度分布趋势由中心向周围递减 ;经典斑中心Aβ沉积最致密 ,周围Aβ沉积最少 ,而斑块外周Aβ沉积密度居中。老年斑三维结构重构方法的建立 ,有助于老年斑积聚动力学的研究 ,并对AD病理机制的探讨具有重要意义。 相似文献
12.
Bone marrow‐derived mesenchymal stem cells (BMMSCs) exhibit degenerative changes, including imbalanced differentiation and reduced proliferation during aging, that contribute to age‐related bone loss. We demonstrate here that autophagy is significantly reduced in aged BMMSCs compared with young BMMSCs. The autophagy inhibitor 3‐methyladenine (3‐MA) could turn young BMMSCs into a relatively aged state by reducing their osteogenic differentiation and proliferation capacity and enhancing their adipogenic differentiation capacity. Accordingly, the autophagy activator rapamycin could restore the biological properties of aged BMMSCs by increasing osteogenic differentiation and proliferation capacity and decreasing adipogenic differentiation capacity. Possible underlying mechanisms were explored, and the analysis revealed that autophagy could affect reactive oxygen species and p53 levels, thus regulating biological properties of BMMSCs. In an in vivo study, we found that activation of autophagy restored bone loss in aged mice. In conclusion, our results suggest that autophagy plays a pivotal role in the aging of BMMSCs, and activation of autophagy could partially reverse this aging and may represent a potential therapeutic avenue to clinically treat age‐related bone loss. 相似文献
13.
Ding ZC Zheng Q Cai B Ni FY Yu WH Teng XC Gao Y Liu F Chen D Wang Y Wu HM Sun HZ Zhang MJ Tan XS Huang ZX 《Journal of inorganic biochemistry》2008,102(11):1965-1972
Human metallothionein-3 (hMT3), also named as human neuronal growth inhibitory factor (hGIF), can inhibit the outgrowth of embryonic cortical neurons in the presence of brain extracts. In order to systematically study the structure-property-reactivity-function relationship of hGIF, our laboratory designed a series of mutants and studied their structure, property, reactivity and functions by a series of chemical and biological tools including UV spectroscopy, CD spectroscopy, NMR, chemical reaction and primary neuronal culture assays. In summary, we concluded that the bioactivity of hGIF was regulated by multiple factors, including the 6CPCP9 motif, an additional threonine insert at sequence position 5, domain-domain interactions, the structure and stability of the metal-thiolate cluster and the linker. Our studies provide more and more evidences which revealed that the bioactivity of hGIF is mainly related to the essential metal release and its characteristic conformation. 相似文献
14.
Ghislaine Le Prince Pia Delaere Christiane Fages Thierry Lefrançois Monique Touret Marcelle Salanon Marcienne Tardy 《Neurochemical research》1995,20(7):859-862
Glutamine synthetase (GS), a metabolic marker of the mature astrocyte, was investigated in the temporal neocortex of postmortem brain samples of 8 cases, either not demented or affected by senile dementia of the Alzheimer type. A negative correlation between the GS protein level and the density of both classical A4 deposits and senile plaques was evidenced. Such a correlation for GS underlies a dysfunction of the astroglial metabolism and particularly of the glutamate and ammonia neutralization. Since GS is sensitive to oxidative lesioning, the changes in GS level that were observed, occurring at the posttranslational stage, might reflect oxidative damage and have severe consequences on the pathological cascade of events. 相似文献
15.
《Biotechnic & histochemistry》2013,88(2):113-120
A method is described for staining nucleoli intensely by treating tissues with formaldehyde, hydrolysing in normal HC1 at 60°C. and staining with aceto-carmine. With correct hydrolysis time, chromosomes and cytoplasm are almost colorless.Formaldehyde increases the acidity of cell parts, especially the nucleolus, presumably by neutralizing the basic protein groups, and increases the resistance to hydrolysis, perhaps by protecting the phospholipoprotein complexes which are most abundant in the nucleolus.Hydrolysis reduces the acidity of cell parts, chiefly by removal of nucleic acids.Aceto-carmine stains cell structures which are weakly acid in character (about pH 4-5) probably by precipitating as large dye aggregates.The technic appears to be highly specific for nucleoli and related cell bodies. 相似文献
16.
Zhihao Chen Ying Huai Gaoyang Chen Shuyu Liu Yan Zhang Dijie Li Fan Zhao Xiaofeng Chen Wenjing Mao Xuehao Wang Chong Yin Chaofei Yang Xia Xu Kang Ru Xiaoni Deng Lifang Hu Yu Li Songlin Peng Ge Zhang Xiao Lin Airong Qian 《International journal of biological sciences》2022,18(13):4837
Senile osteoporosis is one of the major health problems in an aging society. Decreased bone formation due to osteoblast dysfunction may be one of the causes of aging-related bone loss. With increasing evidence suggesting that multiple microRNAs (miRNAs) play important roles in osteoblast function, the relationship between miRNAs and senile osteoporosis has become a popular research topic. Previously, we confirmed that mechanoresponsive miR-138-5p negatively regulated bone anabolic action. In this study, the miR-138-5p level was found to be negatively correlated with BMD and osteogenic markers in bone specimens of senile osteoporotic patients by bioinformatic analysis and experimental verification. Furthermore, high miR-138-5p levels aggravated the decrease of aged osteoblast differentiation in vitro and led to worse bone loss in aged osteoblastic miR-138-5p transgenic mice in vivo. We also previously identified that the target of miR-138-5p, microtubule actin cross-linking factor 1 (MACF1), could attenuate senile osteoporosis. Here, miR-138-5p was demonstrated to regulate aged osteoblast differentiation by targeting MACF1. Finally, the therapeutic inhibition of miR-138-5p counteracted the decrease in bone formation and aging-related bone loss in aged mice. Overall, our results highlight the crucial roles and the molecular mechanism of miR-138-5p in aging-related bone loss and may provide a powerful therapeutic target for ameliorating senile osteoporosis. 相似文献
17.
18.
A. Bigi M.H.J. Koch P.P. Purslow A. Ripamonti N. Roveri Z. Sayers 《International journal of biological macromolecules》1985,7(1):19-24
The structure and distribution of collagen fibres in Metridium senile mesoglea has been investigated using high and small angle X-ray diffraction techniques on conventional and synchrotron sources. The mesoglea collagen axial spacing appears very close to that of rat tail tendon, which is at variance with the values previously obtained from electron microscopic observations. The different intensity distribution of the small angle X-ray diffraction maxima recorded for mesoglea and rat tail tendon indicates a different distribution of electron density inside the repeating period. Furthermore the absence of the first order, the weak second order and the strong third and sixth orders in the patterns of wet and dry mesogleal collagen could explain that only a periodicity of 20–22 nm corresponding to one-third of the true axial period observed in the electron micrographs. The analysis of the reflections at 0.29 and 1.1–1.4 nm characteristics of the collagen molecular structure have been used to determine the distribution and orientation of the collagen fibres in unstretched and stretched samples 相似文献
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20.
表观遗传修饰异常见于人类的多种疾病(如肿瘤、老年性疾病、发育源性疾病等),影响着这些疾病的发生发展。已有的研究表明,异常表观遗传改变可以作为疾病状态和疾病预测的生物标志物。表观遗传修饰改变的可逆性和可控性也为疾病早期的预防和治疗提供了新策略。本文对DNA甲基化修饰、组蛋白共价修饰、非编码RNA等三种表观遗传方式在肿瘤、老年性疾病和发育源性疾病的研究,以及三者作为表遗传生物标志物在疾病早期诊断和治疗的应用展开介绍,以期为肿瘤、老年性和发育源性相关疾病的诊断与治疗提供借鉴和 参考。 相似文献