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68,395 result(s) for "Chen, Hu"
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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.
Global Shanghai remade : the rise of Pudong New Area
\"Examining the rise of Pudong and its role in re-creating Shanghai as a global city, Global Shanghai Remade utilises this important case study to shed light on contemporary globalisation and China's integration with the world since the late 20th century. Unpacking the rise of Pudong in the context of Deng Xiaoping's nation-building agenda, this book explores the development of the district from its earliest planning into a global city centre through multiple perspectives. In doing so, it explores the role of key decision-makers and actors, the strategic planning process, the approaches to urban development, and some of the iconic projects that define the rise of Pudong, Shanghai, and China itself. A timely volume for the 30th anniversary of China's strategy of 'developing and opening Pudong,' it combines the analyses and findings from these perspectives into a framework for a broader understanding of city-making with Chinese characteristics. The first study of its kind, providing a comprehensive and systematic examination of Pudong, this book will be useful for students and scholars of urban planning and design, as well as Chinese Studies and Development Studies more generally\"-- Provided by publisher.
The antimicrobial activity of nanoparticles: present situation and prospects for the future
Nanoparticles (NPs) are increasingly used to target bacteria as an alternative to antibiotics. Nanotechnology may be particularly advantageous in treating bacterial infections. Examples include the utilization of NPs in antibacterial coatings for implantable devices and medicinal materials to prevent infection and promote wound healing, in antibiotic delivery systems to treat disease, in bacterial detection systems to generate microbial diagnostics, and in antibacterial vaccines to control bacterial infections. The antibacterial mechanisms of NPs are poorly understood, but the currently accepted mechanisms include oxidative stress induction, metal ion release, and non-oxidative mechanisms. The multiple simultaneous mechanisms of action against microbes would require multiple simultaneous gene mutations in the same bacterial cell for antibacterial resistance to develop; therefore, it is difficult for bacterial cells to become resistant to NPs. In this review, we discuss the antibacterial mechanisms of NPs against bacteria and the factors that are involved. The limitations of current research are also discussed.
DEMATEL Technique: A Systematic Review of the State-of-the-Art Literature on Methodologies and Applications
Decision making trial and evaluation laboratory (DEMATEL) is considered as an effective method for the identification of cause-effect chain components of a complex system. It deals with evaluating interdependent relationships among factors and finding the critical ones through a visual structural model. Over the recent decade, a large number of studies have been done on the application of DEMATEL and many different variants have been put forward in the literature. The objective of this study is to review systematically the methodologies and applications of the DEMATEL technique. We reviewed a total of 346 papers published from 2006 to 2016 in the international journals. According to the approaches used, these publications are grouped into five categories: classical DEMATEL, fuzzy DEMATEL, grey DEMATEL, analytical network process- (ANP-) DEMATEL, and other DEMATEL. All papers with respect to each category are summarized and analyzed, pointing out their implementing procedures, real applications, and crucial findings. This systematic and comprehensive review holds valuable insights for researchers and practitioners into using the DEMATEL in terms of indicating current research trends and potential directions for further research.
Hormone-Related and Drug-Induced Osteoporosis: A Cellular and Molecular Overview
Osteoporosis resulting from an imbalance of bone turnover between resorption and formation is a critical health issue worldwide. Estrogen deficiency following a nature aging process is the leading cause of hormone-related osteoporosis for postmenopausal women, while glucocorticoid-induced osteoporosis remains the most common in drug-induced osteoporosis. Other medications and medical conditions related to secondary osteoporosis include proton pump inhibitors, hypogonadism, selective serotonin receptor inhibitors, chemotherapies, and medroxyprogesterone acetate. This review is a summary of the cellular and molecular mechanisms of bone turnover, the pathophysiology of osteoporosis, and their treatment. Nuclear factor-κβ ligand (RANKL) appears to be the critical uncoupling factor that enhances osteoclastogenesis. In contrast, osteoprotegerin (OPG) is a RANKL antagonist secreted by osteoblast lineage cells. Estrogen promotes apoptosis of osteoclasts and inhibits osteoclastogenesis by stimulating the production of OPG and reducing osteoclast differentiation after suppression of IL-1 and TNF, and subsequent M-CSF, RANKL, and IL-6 release. It can also activate the Wnt signaling pathway to increase osteogenesis, and upregulate BMP signaling to promote mesenchymal stem cell differentiation from pre-osteoblasts to osteoblasts rather than adipocytes. Estrogen deficiency leads to the uncoupling of bone resorption and formation; therefore, resulting in greater bone loss. Excessive glucocorticoids increase PPAR-2 production, upregulate the expression of Dickkopf-1 (DKK1) in osteoblasts, and inhibit the Wnt signaling pathway, thus decreasing osteoblast differentiation. They promote osteoclast survival by enhancing RANKL expression and inhibiting OPG expression. Appropriate estrogen supplement and avoiding excessive glucocorticoid use are deemed the primary treatment for hormone-related and glucocorticoid-induced osteoporosis. Additionally, current pharmacological treatment includes bisphosphonates, teriparatide (PTH), and RANKL inhibitors (such as denosumab). However, many detailed cellular and molecular mechanisms underlying osteoporosis seem complicated and unexplored and warrant further investigation.
Fecal Calprotectin in Predicting Relapse of Inflammatory Bowel Diseases: A Meta-analysis of Prospective Studies
Fecal calprotectin (FC) is a relatively new marker of intestinal inflammation. Recently, many studies have extended its role in predicting relapse of quiescent inflammatory bowel disease (IBD), but the reported results have been inconsistent. We aimed to perform a meta-analysis of the predictive capacity of FC in IBD relapse.MethodsWe systematically searched the Medline, Web of Science, Cochrane Library, and EMBASE databases for prospective studies that used FC concentrations at remission in predicting relapse of Crohn's disease (CD) and ulcerative colitis (UC). Pooled sensitivity, specificity, and other diagnostic indices were evaluated.ResultsA total of 672 IBD patients (318 UC and 354 CD) from six different studies were analyzed. The pooled sensitivity and specificity of FC to predict relapse of quiescent IBD was 78% (95% confidence interval [CI]: 72–83) and 73% (95% CI: 68–77), respectively. The area under the summary receiver-operating characteristic (sROC) curve was 0.83 and the diagnostic odds ratio was 10.31 (95% CI: 5.05–21.06). The capacity of FC to predict relapse was comparable between UC and CD. In CD patients the predictive value of FC in isolated small bowel CD was not assessed due to insufficiency of available data. Compared with all enrolled CD patients, FC appeared to be more accurate in ileocolonic and colonic CD.ConclusionsAs a simple and noninvasive marker, FC is useful to predict relapse in quiescent IBD patients.
Isoflavone Supplements for Menopausal Women: A Systematic Review
Isoflavones have gained popularity as an alternative treatment for menopausal symptoms for people who cannot or are unwilling to take hormone replacement therapy. However, there is still no consensus on the effects of isoflavones despite over two decades of vigorous research. This systematic review aims to summarize the current literature on isoflavone supplements, focusing on the active ingredients daidzein, genistein, and S-equol, and provide a framework to guide future research. We performed a literature search in Ovid Medline using the search terms “isoflavone” and “menopause”, which yielded 95 abstracts and 68 full-text articles. We found that isoflavones reduce hot flashes even accounting for placebo effect, attenuate lumbar spine bone mineral density (BMD) loss, show beneficial effects on systolic blood pressure during early menopause, and improve glycemic control in vitro. There are currently no conclusive benefits of isoflavones on urogenital symptoms and cognition. Due to the lack of standardized research protocols including isoflavone component and dosage, outcomes, and trial duration, it is difficult to reach a conclusion at this point in time. Despite these limitations, the evidence thus far favors the use of isoflavones due to their safety profile and benefit to overall health.
Important contributions of non-fossil fuel nitrogen oxides emissions
Since the industrial revolution, it has been assumed that fossil-fuel combustions dominate increasing nitrogen oxide (NO x ) emissions. However, it remains uncertain to the actual contribution of the non-fossil fuel NO x to total NO x emissions. Natural N isotopes of NO 3 − in precipitation (δ 15 N w-NO3− ) have been widely employed for tracing atmospheric NO x sources. Here, we compiled global δ 15 N w-NO3− observations to evaluate the relative importance of fossil and non-fossil fuel NO x emissions. We found that regional differences in human activities directly influenced spatial-temporal patterns of δ 15 N w-NO3− variations. Further, isotope mass-balance and bottom-up calculations suggest that the non-fossil fuel NO x accounts for 55 ± 7% of total NO x emissions, reaching up to 21.6 ± 16.6Mt yr −1 in East Asia, 7.4 ± 5.5Mt yr −1 in Europe, and 21.8 ± 18.5Mt yr −1 in North America, respectively. These results reveal the importance of non-fossil fuel NO x emissions and provide direct evidence for making strategies on mitigating atmospheric NO x pollution. This study investigates in the importance of non-fossil fuel NO x emissions in the surface-earth-nitrogen cycle. The study shows how changes of regional human activities directly influence δ 15 N signatures of deposited NO x to terrestrial environments and that emissions have largely been underestimated.
The Molecular and Cellular Mechanisms of Endometriosis: From Basic Pathophysiology to Clinical Implications
Endometriosis is a complex gynecological disorder characterized by endometrial-like tissue growing outside the uterus, leading to chronic pain, infertility, and reduced quality of life. Its pathophysiology involves genetic, epigenetic, immune, and molecular factors. Theories such as retrograde menstruation, coelomic metaplasia, and stem cell involvement explain lesion formation. Endometrial mesenchymal stem cells (eMSCs) and epithelial progenitors (eEPs) contribute to lesion establishment by adhering to peritoneal surfaces, proliferating, and differentiating into ectopic tissue. Aberrant adhesion molecules, inflammatory cytokines, and molecular pathways like PI3K/Akt and Wnt/β-catenin drive proliferation, angiogenesis, and resistance to apoptosis. Elevated estrogen levels and progesterone resistance further promote lesion growth and immune evasion. Immune dysfunction, including altered macrophage activity and reduced natural killer (NK) cell function, contributes to inflammation and lesion persistence. Pain is linked to prostaglandin E2 (PGE2) and nerve infiltration, emphasizing the need for targeted pain management. Current therapies, such as GnRH agonists, suppress ovarian hormone production but face limitations in long-term efficacy and side effects. Integrating molecular insights into clinical practice may advance diagnostics and treatment, with emerging approaches focusing on molecular pathways, immune modulation, and hormonal regulation for more effective, personalized therapies. Future research should unravel the complex mechanisms driving endometriosis to improve patient outcomes.