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In order to test to what degree Schmorl's nodes (SN), osteophytosis of the vertebral bodies (VO), and osteoarthritis of the articular facets (OA) are useful indicators of activity-related stress, an analysis of their frequencies and severity of expression was conducted in two early Modern period skeletal samples from Croatia--Koprivno and Sisak. Historic and contemporary ethnographic sources suggest that living conditions were more demanding in Koprivno, and that a sexual division of labor existed in both populations. A total of 2,552 vertebral bodies (990 from Koprivno and 1,562 from Sisak) and 5,186 articular facets (2,135 from Koprivno and 3,051 from Sisak) were analyzed. Koprivno exhibits significantly higher total frequencies of SN, VO, and OA than Sisak, and the total frequencies of SN and OA in both series are significantly higher in males. When, however, the series were analyzed by age and sex categories, the same trend was noted only in SN. The frequencies and severity of VO and OA could not be interpreted in keeping with the historic and contemporary ethnographic sources and were additionally, unlike SN, found to be strongly correlated with increased age. This study, therefore, suggests that while SN are useful indicators of different lifestyles and/or different activity patterns between various archaeological populations, VO and OA are-possibly because of their more varied etiologies-less useful markers of activity-related stress. 相似文献
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The transformation of polypeptide chains from their globular native structure to fibrillar aggregates has been a matter of great concern because of the involvement of these aggregates in the onset of several degenerative diseases. These aggregates exhibit highly ordered cross β sheet structures and are known as ‘amyloids’. Formation of amyloids in the body is associated with cytotoxicity due to direct interaction of the aggregated species with the cell membrane leading to cellular permeability or due to loss of functionality of the proteins involved in the amyloid formation. The preference of polypeptide chains to remain in their native conformation or to aggregate into amyloids is guided by several factors such as its conformation at specific condition, concentration, physicochemical properties of the amino acid sequence and so on. In the current review, we have reviewed the different factors that guide the transition of proteins from their natively folded state to the amyloidogenic state. Understanding the critical determinants of amyloidogenesis is vital towards deciphering the molecular mechanism of amyloidogenesis and for the development of effective therapeutics against amyloidosis. Copyright © 2013 European Peptide Society and John Wiley & Sons, Ltd. 相似文献
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椎间盘退变始发于髓核组织,获得足够有功能的髓核细胞是研究及治疗椎间盘退变的关键.而人诱导多能干细胞(induced pluripotent stem cell,iPSC)不仅为建立疾病模型以研究疾病发生发展机制开辟了道路,还在再生医学领域展现出了广阔的应用前景.我们首先从椎间盘退变患者微创手术获得的髓核组织内分离髓核细胞,将携带OCT3/4、SOX2、KLF4和c-MYC的仙台病毒(Sendai virus,Se V)转染髓核细胞,重编程获得iPSC.通过检测多能细胞特异性标志、体内成瘤实验、甲基化及核型分析对所获得的iPSC进行鉴定.并以皮肤成纤维细胞来源iPSC作为对照,在二维和三维水凝胶中对iPSC进行定向分化,检测髓核细胞相关蛋白和基因的表达,比较分析2种iPSC向髓核细胞的分化效率.结果显示,iPSC能表达多能细胞特异性标志,具有正常的二倍体核型,畸胎瘤实验显示三个胚层的出现.诱导分化后的iPSC表达髓核相关基因和蛋白,在水凝胶中诱导培养后,iPSC表达更多的髓核相关基因和蛋白.髓核来源的iPSC与成纤维细胞来源的iPSC相比,可表达更多的髓核相关基因和蛋白.本研究首次将患者退变髓核细胞重编程成iPSC,并在水凝胶内将其诱导分化为髓核样细胞,为椎间盘退变个体化细胞治疗奠定基础. 相似文献
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Qi Zhang Xi-min Hu Wen-juan Zhao Xiao-xia Ban Yan Li Yan-xia Huang Hao Wan Ye He Lv-shuang Liao Lei Shang Bin Jiang Guo-ping Qing Kun Xiong 《International journal of biological sciences》2023,19(2):658
The discovery of the necroptosis, a form of regulated necrosis that is mediated by receptor-interacting protein kinase 1 (RIPK1), RIPK3, and mixed-lineage kinase domain-like pseudokinase (MLKL), represents a major breakthrough that has dramatically altered the conception of necrosis - traditionally thought of as uncontrolled cell death - in various human diseases. Retinal cell death is a leading cause of blindness and has been identified in most retinal diseases, e.g., age-related macular degeneration, glaucoma, retinal detachment, retinitis pigmentosa, etc. Increasing evidence demonstrates that retinal degenerative diseases also share a common mechanism in necroptosis. Exacerbated necroptotic cell death hinders the treatment for retinal degenerative diseases. In this review, we highlight recent advances in identifying retinal necroptosis, summarize the underlying mechanisms of necroptosis in retinal degenerative diseases, and discuss potential anti-necroptosis strategies, such as selective inhibitors and chemical agents, for treating retinal degenerative diseases. 相似文献
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Manipulation of human diet can modulate urinary biomarkers of oxidative DNA base damage (UBODBD), reflecting changes in levels of DNA damage. When dietary composition is maintained but caloric intake is decreased (caloric restriction), UBODBD excretion is suppressed. At isocaloric dietary intake the level of damage depends on diet composition. For diets consisting of foods containing carbohydrates, proteins, and fats but lacking fruits and vegetables, the level of damage is higher than for diets including fruits and vegetables, which are rich in natural antioxidants. Assay of urinary biomarkers is suggested as a potential test for quantitative assessment of the carcinogenic or anticarcinogenic properties of foods, food components, and diets and for individual responses to nutritional regimens. 相似文献
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Anthony T. Diplock 《Free radical research》1997,26(6):565-583
Recent research about the role of free radical derivatives of oxygen and nitrogen in biological systems has highlighted the possibility that antioxidants, such as vitamin E, that prevent these processes in vitro may be capable of carrying out a similar function in living organisms in vivo. There is increasing evidence that free radical reactions are involved in the early stages, or sometimes later on, in the development of human diseases, and it is therefore of particular interest to inquire whether vitamin E and other antioxidants, which are found in the human diets, may be capable of lowering the incidence of these diseases. Put simply, the proposition is that by improving human diets by increasing the quantity in them of antioxidants, it might be possible to reduce the incidence of a number of degenerative diseases. Of particular significance to these considerations is the likely role of the primary fat-soluble dietary antioxidant vitamin E in the prevention of degenerative diseases such as arteriosclerosis, which is frequently the cause of consequent heart attacks or stroke, and prevention of certain forms of cancer, as well as several other diseases. Substantial evidence for this proposition now exists, and this review is an attempt to give a brief account of the present position. Two kinds of evidence exist; on the one hand there is very substantial basic science evidence which indicates an involvement of free radical events, and a preventive role for vitamin E, in the development of human disease processes. On the other hand, there is also a large body of human epidemiological evidence which suggests that incidence of these diseases is lowered in populations having a high level of antioxidants, such as vitamin E, in their diet, or who have taken steps to enhance their level of intake of the vitamin by taking dietary supplements. There is also some evidence which suggests that intervention with dietary supplements of vitamin E can result in a lowered risk of disease, in particular of cardiovascular disease, which is a major killer disease among the developed nations of the world. The intense interest in this subject recently has as its objective the possibility that, by making some simple alterations to dietary lifestyle, or by enhancing the intake of vitamin E by fortification of foods, or by dietary supplements, it may be possible to reduce substantially the risk of a large amount of common, highly disabling human disease. By this simple means, therefore it may be possible to improve substantially the quality of human life, in particular for people of advancing years. 相似文献
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Franca Scanabissi Michele Cesari Sadie K. Reed Stephen C. Weeks 《Invertebrate Biology》2006,125(2):117-124
Abstract. The ultrastructure of the male gonad of Eulimnadia texana (Branchiopoda, Spinicaudata) has been observed for the first time to investigate the sexuality of a well-studied case of androdioecy in the animal kingdom. The male gonad is a double structure located in the hemocoel throughout the entire body length on each side of the midgut. Male gametes originate from the wall and mature centripetally toward the lumen; the proliferative activity is very high and continuous and therefore the mature gonad is full of numerous germ cells. Inside the lumen several degenerative stages are found mixed with sperm cells and spermatids, the latter two being not easily distinguishable because of the slight differences between them. The evolutionary meaning of the degenerative process in E. texana male gametes is difficult to explain, and we propose some hypotheses about its possible role or cause in the studied population: (a) to help build spermatophores, (b) to act as a trophic component for viable sperm, (c) as a manifestation of inbreeding depression, and/or (d) to regulate the number of sperm cells. 相似文献
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Jose Antonio Sánchez Milán María Fernández-Rhodes Xue Guo María Mulet SoFong Cam Ngan Ranjith Iyappan Maryam Katoueezadeh Siu Kwan Sze Aida Serra Xavier Gallart-Palau 《Aging cell》2024,23(3):e14062
Aging is the primary risk factor for the development of numerous human chronic diseases. On a molecular level, it significantly impacts the regulation of protein modifications, leading to the accumulation of degenerative protein modifications (DPMs) such as aberrant serine phosphorylation (p-Ser) and trioxidized cysteine (t-Cys) within the proteome. The altered p-Ser is linked to abnormal cell signaling, while the accumulation of t-Cys is associated with chronic diseases induced by oxidative stress. Despite this, the potential cross-effects and functional interplay between these two critical molecular factors of aging remain undisclosed. This study analyzes the aging proteome of wild-type C57BL/6NTac mice over 2 years using advanced proteomics and bioinformatics. Our objective is to provide a comprehensive analysis of how t-Cys affects cell signaling and protein structure in the aging process. The results obtained indicate that t-Cys residues accumulate in the aging proteome, interact with p-Ser interacting enzymes, as validated in vitro, and alter their structures similarly to p-Ser. These findings have significant implications for understanding the interplay of oxidative stress and phosphorylation in the aging process. Additionally, they open new venues for further research on the role(s) of these protein modifications in various human chronic diseases and aging, wherein exacerbated oxidation and aberrant phosphorylation are implicated. 相似文献