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The inhibition by human MSCs-derived miRNA-124a overexpression exosomes in the proliferation and migration of rheumatoid arthritis-related fibroblast-like synoviocyte cell
Background
Rheumatoid arthritis is a long-term, progressive autoimmune disease. It is characterized by synovial hyperplasia leading to swelling, stiffness, and joint deformity in more than one joint. Fibroblast-like synoviocytes are the major cell types that make up the synovial intima structure, which is one of the decisive factors in the development and course of rheumatoid arthritis.
Methods
The potential therapeutic effects of MSCs-derived miRNA-124a overexpression exosomes were evaluated in vitro by the method including MTT assay and cell cycle test for cell proliferation, scratch wound closure and transwell for cell migration, flow cytometry and western for the apoptosis detection.
Results
Exosomes derived from human MSCs that overexpression miRNA-124a were prepared and characterized. We found that the pretreatment of this exosome was able to inhibit the proliferation and migration of fibroblast-like synoviocyte cell line and promote the apoptosis of this cell during the co-incubation.
Conclusions
Exosomes derived from MSCs were proved to be a suitable vector for the delivery of therapeutic miRNA-124a, and such miRNA-124a overexpression exosomes were expected to provide a new medicine and strategy for the treatment of rheumatoid arthritis.
Journal Article
The archaeology of China : from the late paleolithic to the early bronze age
\"Past, present and future \"The archaeological materials recovered from the Anyang excavations ... in the period between 1928 and 1937...have laid a new foundation for the study of ancient China (Li, C. 1977: ix).\" When inscribed oracle bones and enormous material remains were found through scientific excavation in Anyang in 1928, the historicity of the Shang dynasty was confirmed beyond dispute for the first time (Li, C. 1977: ix-xi). This excavation thus marked the beginning of a modern Chinese archaeology endowed with great potential to reveal much of China's ancient history.. Half a century later, Chinese archaeology had made many unprecedented discoveries which surprised the world, leading Glyn Daniel to believe that \"a new awareness of the importance of China will be a key development in archaeology in the decades ahead (Daniel 1981: 211). This enthusiasm was soon shared by the Chinese archaeologists when Su Bingqi announced that \"the Golden Age of Chinese archaeology is arriving (Su, B. 1994: 139--140)\". In recent decades, archaeology has continuously prospered, becoming one of the most rapidly developing fields in social science in China\"-- Provided by publisher.
Book
Osteoporosis Due to Hormone Imbalance: An Overview of the Effects of Estrogen Deficiency and Glucocorticoid Overuse on Bone Turnover
Osteoporosis is a serious health issue among aging postmenopausal women. The majority of postmenopausal women with osteoporosis have bone loss related to estrogen deficiency. The rapid bone loss results from an increase in bone turnover with an imbalance between bone resorption and bone formation. Osteoporosis can also result from excessive glucocorticoid usage, which induces bone demineralization with significant changes of spatial heterogeneities of bone at microscale, indicating potential risk of fracture. This review is a summary of current literature about the molecular mechanisms of actions, the risk factors, and treatment of estrogen deficiency related osteoporosis (EDOP) and glucocorticoid induced osteoporosis (GIOP). Estrogen binds with estrogen receptor to promote the expression of osteoprotegerin (OPG), and to suppress the action of nuclear factor-κβ ligand (RANKL), thus inhibiting osteoclast formation and bone resorptive activity. It can also activate Wnt/β-catenin signaling to increase osteogenesis, and upregulate BMP signaling to promote mesenchymal stem cell differentiation from pre-osteoblasts to osteoblasts, rather than adipocytes. The lack of estrogen will alter the expression of estrogen target genes, increasing the secretion of IL-1, IL-6, and tumor necrosis factor (TNF). On the other hand, excessive glucocorticoids interfere the canonical BMP pathway and inhibit Wnt protein production, causing mesenchymal progenitor cells to differentiate toward adipocytes rather than osteoblasts. It can also increase RANKL/OPG ratio to promote bone resorption by enhancing the maturation and activation of osteoclast. Moreover, excess glucocorticoids are associated with osteoblast and osteocyte apoptosis, resulting in declined bone formation. The main focuses of treatment for EDOP and GIOP are somewhat different. Avoiding excessive glucocorticoid use is mandatory in patients with GIOP. In contrast, appropriate estrogen supplement is deemed the primary treatment for females with EDOP of various causes. Other pharmacological treatments include bisphosphonate, teriparatide, and RANKL inhibitors. Nevertheless, more detailed actions of EDOP and GIOP along with the safety and effectiveness of medications for treating osteoporosis warrant further investigation.
Journal Article
Systemic adaptation of lipid metabolism in response to low‐ and high‐fat diet in Nile tilapia (Oreochromis niloticus)
Natural selection endows animals with the abilities to store lipid when food is abundant and to synthesize lipid when it is limited. However, the relevant adaptive strategy of lipid metabolism has not been clearly elucidated in fish. This study examined the systemic metabolic strategies of Nile tilapia to maintain lipid homeostasis when fed with low‐ or high‐fat diets. Three diets with different lipid contents (1%, 7%, and 13%) were formulated and fed to tilapias for 10 weeks. At the end of the feeding trial, the growth rate, hepatic somatic index, and the triglyceride (TG) contents of serum, liver, muscle, and adipose tissue were comparable among three groups, whereas the total body lipid contents and the mass of adipose tissue increased with the increased dietary lipid levels. Overall quantitative PCR, western blotting and transcriptomic assays indicated that the liver was the primary responding organ to low‐fat (LF) diet feeding, and the elevated glycolysis and accelerated biosynthesis of fatty acids (FA) in the liver is likely to be the main strategies of tilapia toward LF intake. In contrast, excess ingested lipid was preferentially stored in adipose tissue through increasing the capability of FA uptake and TG synthesis. Increasing numbers, but not enlarging size, of adipocytes may be the main strategy of Nile tilapia responding to continuous high‐fat (HF) diet feeding. This is the first study illuminating the systemic adaptation of lipid metabolism responding to LF or HF diet in fish, and our results shed new light on fish physiology. We illustrated the adaptive strategy of lipid metabolism responding to low or high fat diets in Nile tilapia. Briefly, the elevated glycolysis and accelerated biosynthesis of fatty acids in the liver were the main strategies of tilapia towards low fat intake. Increasing numbers, but not enlarging size, of adipocytes was the main strategy of Nile tilapia responding to continuous high‐fat diet feeding.
Journal Article
External powers and the Gulf monarchies
The Gulf monarchies have been generally perceived as status quo actors reliant on the USA for their security, but in response to regional events, particularly the Arab Spring of 2011, they are pursuing more activist foreign policies, which has allowed other international powers to play a larger role in regional affairs. This book analyses the changing dynamic in this region, with expert contributors providing original empirical case studies that examine the relations between the Gulf monarchies and extra-regional powers, including the USA, Russia, China, India, Brazil, Turkey, Japan, South Korea, France, and the United Kingdom. At the theoretical level, these case studies explore the extent to which different international relations and international political economy theories explain change in these relationships as the regional, political and security environment shifts. Focusing on how and why external powers approach their relationships with the Gulf monarchies, contributors ask what motivates external powers to pursue deeper involvement in an unstable region that has seen three major conflicts in the past 40 years. -- Publisher description.
Book
C(sp3)−C(sp3) bond formation via nickel-catalyzed deoxygenative homo-coupling of aldehydes/ketones mediated by hydrazine
Aldehydes and ketones are widely found in biomass resources and play important roles in organic synthesis. However, the direct deoxygenative coupling of aldehydes or ketones to construct C(sp
3
)−C(sp
3
) bond remains a scientific challenge. Here we report a nickel−catalyzed reductive homo-coupling of moisture- and air-stable hydrazones generated in-situ from naturally abundant aldehydes and ketones to construct challenging C(sp
3
)−C(sp
3
) bond. This transformation has great functional group compatibility and can suit a broad substrate scope with innocuous H
2
O, N
2
and H
2
as the by-products. Furthermore, the application in several biological molecules and the transformation of PEEK model demonstrate the generality, practicability, and applicability of this novel methodology.
The direct deoxygenative coupling of aldehydes or ketones to construct C(sp
3
)−C(sp
3
) bond remains a scientific challenge. Here the authors use a nickel−catalyzed reductive homo-coupling of moisture- and air-stable hydrazones generated in-situ from naturally abundant aldehydes and ketones to construct challenging C(sp
3
)−C(sp
3
) bonds.
Journal Article
System Xc−/GSH/GPX4 axis: An important antioxidant system for the ferroptosis in drug-resistant solid tumor therapy
The activation of ferroptosis is a new effective way to treat drug-resistant solid tumors. Ferroptosis is an iron-mediated form of cell death caused by the accumulation of lipid peroxides. The intracellular imbalance between oxidant and antioxidant due to the abnormal expression of multiple redox active enzymes will promote the produce of reactive oxygen species (ROS). So far, a few pathways and regulators have been discovered to regulate ferroptosis. In particular, the cystine/glutamate antiporter (System X c − ), glutathione peroxidase 4 (GPX4) and glutathione (GSH) (System X c − /GSH/GPX4 axis) plays a key role in preventing lipid peroxidation-mediated ferroptosis, because of which could be inhibited by blocking System X c − /GSH/GPX4 axis. This review aims to present the current understanding of the mechanism of ferroptosis based on the System X c − /GSH/GPX4 axis in the treatment of drug-resistant solid tumors.
Journal Article