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1.
Experimental study on the impact of "IDS + JFCS" complex wetting agent on the characteristics of coal bodies.
Wang, H, Xu, L, Qin, Z, Li, X, Cao, X, Han, Y, Li, S, Ma, Y, Gao, S, Du, L, et al
Scientific reports. 2024;(1):7163
Abstract
As China's coal mines have transitioned to deep mining, the ground stress within the coal seams has progressively increased, resulting in reduced permeability and poor wetting ability of conventional wetting agents. Consequently, these agents have become inadequate in fulfilling the requirements for preventing washouts during deep mining operations. In response to the aforementioned challenges, a solution was proposed to address the issues by formulating a composite wetting agent. This composite wetting agent combines a conventional surfactant with a chelating agent called tetrasodium iminodisuccinate (IDS). By conducting a meticulous screening of surfactant monomer solutions, the ideal formulation for the composite wetting agent was determined by combining the monomer surfactant with IDS. Extensive testing, encompassing evaluations of the composite solution's apparent strain, contact angle measurements, and alterations in the oxygenated functional groups on the coal surface, led to the identification of the optimal composition. This composition consisted of IDS serving as the chelating agent and fatty alcohol polyoxyethylene ether (JFCS).Subsequent assessment of the physical and mechanical performance of the coal briquettes treated with the composite wetting agent revealed notable enhancements. These findings signify significant advancements in the field and hold promising implications. Following the application of the composite wetting agent, notable reductions were observed in the dry basis ash and dry basis full sulfur of coal. Additionally, the water content within the coal mass increased significantly, leading to a substantial enhancement in the wetting effect of the coal body. This enhanced wetting effect effectively mitigated the coal body's inclination towards impact, thereby offering technical support for optimizing water injection into coal seams and preventing as well as treating impact ground pressure.
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2.
Effects of Helicobacter pylori Therapy on Gut Microbiota: A Systematic Review and Meta-Analysis.
Du, L, Chen, B, Cheng, F, Kim, J, Kim, JJ
Digestive diseases (Basel, Switzerland). 2024;(1):102-112
Abstract
BACKGROUND Although indications for evaluation and treatment of Helicobacter pylori infection are broadening to include primary prevention for gastric adenocarcinoma, potential adverse effects on gut microbiota have been raised. We performed a systematic review and meta-analysis to evaluate the effects of H. pylori therapy on gut microbiota. METHODS PubMed, EMBASE, Cochrane Library, and Web of Science (to 4/2021) were searched for studies quantitatively evaluating microbiota before and after H. pylori therapy. Meta-analysis was performed to assess early (<1 year) and long-term (≥1 year) effects on gut microbiota after H. pylori treatment. Subgroup analysis evaluating the effects of H. pylori therapy with addition of probiotics on gut microbiota was also performed. RESULTS Thirty studies (N = 1,218) met the criteria. Early after H. pylori therapy, intestinal microbial diversity was reduced in nearly all studies. At the genus level, reduction in the abundance of Enterococcus, while increase in Lactobacillus, Bifidobacterium, and Bacteroides counts were observed. However, Enterococcus, Lactobacillus, Bifidobacterium, and Bacteroides counts remained stable in patients who received probiotics with H. pylori therapy. At the phylum level, the relative abundance of Actinobacteria and Firmicutes increased after treatment. At ≥1 year, intestinal microbial diversity normalized in six of seven studies. No differences in the relative abundance of Actinobacteria, Firmicute, Bacteroidetes, and Proteobacteria were observed ≥1 year after therapy. CONCLUSION The impact of H. pylori therapy on gut microbiota appears transient with early changes largely resolving after 1 year. Probiotics may reduce the early impact of H. pylori therapy on gut microbiota.
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3.
Impact of Cholesterol Metabolism on H2O2-Induced Oxidative Stress Injury in HepG2 Cells Treated with Fatty Acids.
Tang, Q, Du, L, Sun, Q
Alternative therapies in health and medicine. 2024;(1):396-402
Abstract
OBJECTIVE This study aimed to evaluate the expression of genes involved in cholesterol metabolism and establish their association with oxidative stress (OS). METHODS We employed an in vitro experimental design and cells were divided into six groups: C (control), CH (HepG2 + H2O2), CHN (HepG2 + H2O2 + NAC), F (FFA-treated HepG2), FH (FFA-treated HepG2 + H2O2), and FHN (FFA-treated HepG2 + H2O2 + NAC). Cell viability was assessed using the MTT assay, while successful FFA model establishment was confirmed via Oil Red staining and absorbance. Oxidative stress injury was gauged by measuring ROS, SOD activity, and MDA content. RNA transcription and protein expression of cholesterol-related (DHCR24, DHCR7) and oxidative stress-related (NFE2L2, HMOX1) genes were also examined via RT-qPCR and WB. RESULTS The impact of H2O2 on cell viability exhibited a time-dose-dependent pattern, paralleling the changes in reactive oxygen species (ROS) levels. Compared to the C group, FFA treatment led to an increase in Oil Red absorption and MDA content and decreased SOD activity. However, it did not result in a significant reduction in cell viability. The FH group exhibited reduced cell viability and SOD activity, along with a further elevation in MDA content compared to the F group. Furthermore, the increased SOD activity and decreased MDA content observed in the CH group were effectively reversed following NAC treatment. Such a reversal was not evident between the FHN and FH groups. Compared to the control group, genes associated with cholesterol metabolism and oxidative stress (OS) displayed heightened expression levels in the other treatment groups, with the FHN group showing lower expression levels than the FH group. Notably, changes in the protein expressions of DHCR24, DHCR7, NFE2L2, and HMOX1 were consistent and exhibited correlations. CONCLUSIONS Cholesterol metabolism emerges as a potential mechanism underlying H2O2-induced oxidative stress injury in HepG2 cells treated with FFA.
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4.
OTUB1/NDUFS2 axis promotes pancreatic tumorigenesis through protecting against mitochondrial cell death.
Huang, XD, Du, L, Cheng, XC, Lu, YX, Liu, QW, Wang, YW, Liao, YJ, Lin, DD, Xiao, FJ
Cell death discovery. 2024;(1):190
Abstract
Pancreatic cancer is one of the most fatal cancers in the world. A growing number of studies have begun to demonstrate that mitochondria play a key role in tumorigenesis. Our previous study reveals that NDUFS2 (NADH: ubiquinone oxidoreductase core subunit S2), a core subunit of the mitochondrial respiratory chain complex I, is upregulated in Pancreatic adenocarcinoma (PAAD). However, its role in the development of PAAD remains unknown. Here, we showed that NDUFS2 played a critical role in the survival, proliferation and migration of pancreatic cancer cells by inhibiting mitochondrial cell death. Additionally, protein mass spectrometry indicated that the NDUFS2 was interacted with a deubiquitinase, OTUB1. Overexpression of OTUB1 increased NDUFS2 expression at the protein level, while knockdown of OTUB1 restored the effects in vitro. Accordingly, overexpression and knockdown of OTUB1 phenocopied those of NDUFS2 in pancreatic cancer cells, respectively. Mechanically, NDUFS2 was deubiquitinated by OTUB1 via K48-linked polyubiquitin chains, resulted in an elevated protein stability of NDUFS2. Moreover, the growth of OTUB1-overexpressed pancreatic cancer xenograft tumor was promoted in vivo, while the OTUB1-silenced pancreatic cancer xenograft tumor was inhibited in vivo. In conclusion, we revealed that OTUB1 increased the stability of NDUFS2 in PAAD by deubiquitylation and this axis plays a pivotal role in pancreatic cancer tumorigenesis and development.
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5.
Time-dependent risk of fracture in adults with type 2 diabetes receiving anti-diabetic drug: A one-stage network meta-analysis.
Shen, Y, Shi, Q, Zou, X, Meng, W, Tian, H, Du, L, Li, S
Diabetes/metabolism research and reviews. 2024;(2):e3780
Abstract
AIMS: To assess the time-dependent risk of fracture in adults with type 2 diabetes receiving anti-diabetic drugs. MATERIALS AND METHODS We searched MEDLINE, EMBASE, and Cochrane Library up to 18 November 2021, for randomized controlled trials (RCTs) and propensity-score-matched non-randomized studies (NRSs) comparing all anti-diabetic drugs with standard treatment or with each other on fracture in adults with type 2 diabetes. The study performed a one-stage network meta-analysis using discrete-time hazard regression with reconstructed individual time-to-event data. RESULTS This network meta-analysis involved seven RCTs (65,051 adults with type 2 diabetes) with a median follow-up of 36 months and three propensity-score-based NRSs (17,954 participants) with a median follow-up of 27.3 months. Among anti-diabetic drugs, thiazolidinediones increased the overall hazard of fracture by 42% (95% credible interval [CrI], 3%-97%) and almost tripled the risk after 4 years (hazard ratio [HR], 2.74; 95% CrI, 1.53-4.80). Credible subgroup analysis suggested that thiazolidinediones increased the hazard of fracture only in females (HR, 2.19; 95% CrI, 1.26-3.74) but not among males (HR, 0.81; 95% CrI, 0.45-1.40). Moderate certainty evidence established that thiazolidinediones increase 92 fractures in five years per 1000 female patients. We did not find the risk of fractures with other anti-diabetic drugs including metformin, sulfonylureas, sodium-glucose cotransporter-2 (SGLT2) inhibitors, and dipeptidyl peptidase-4 (DPP-4) inhibitors. CONCLUSIONS Long-term use of thiazolidinediones elevates the risk of fracture among females with type 2 diabetes. There is no evidence eliciting fracture risk associated with other anti-diabetic drugs.
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6.
The critical role of toll-like receptor 4 in bone remodeling of osteoporosis: from inflammation recognition to immunity.
Zhu, X, Du, L, Zhang, L, Ding, L, Xu, W, Lin, X
Frontiers in immunology. 2024;:1333086
Abstract
Osteoporosis is a common chronic metabolic bone disorder. Recently, increasing numbers of studies have demonstrated that Toll-like receptor 4 (TLR4, a receptor located on the surface of osteoclasts and osteoblasts) plays a pivotal role in the development of osteoporosis. Herein, we performed a comprehensive review to summarize the findings from the relevant studies within this topic. Clinical data showed that TLR4 polymorphisms and aberrant TLR4 expression have been associated with the clinical significance of osteoporosis. Mechanistically, dysregulation of osteoblasts and osteoclasts induced by abnormal expression of TLR4 is the main molecular mechanism underlying the pathological processes of osteoporosis, which may be associated with the interactions between TLR4 and NF-κB pathway, proinflammatory effects, ncRNAs, and RUNX2. In vivo and in vitro studies demonstrate that many promising substances or agents (i.e., methionine, dioscin, miR-1906 mimic, artesunate, AEG-1 deletion, patchouli alcohol, and Bacteroides vulgatus) have been able to improve bone metabolism (i.e., inhibits bone resorption and promotes bone formation), which may partially attribute to the inhibition of TLR4 expression. The present review highlights the important role of TLR4 in the clinical significance and the pathogenesis of osteoporosis from the aspects of inflammation and immunity. Future therapeutic strategies targeting TLR4 may provide a new insight for osteoporosis treatment.
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7.
Senkyunolide I: A Review of Its Phytochemistry, Pharmacology, Pharmacokinetics, and Drug-Likeness.
Huang, Y, Wu, Y, Yin, H, Du, L, Chen, C
Molecules (Basel, Switzerland). 2023;(8)
Abstract
Senkyunolide I (SI) is a natural phthalide that has drawn increasing interest for its potential as a cardio-cerebral vascular drug candidate. In this paper, the botanical sources, phytochemical characteristics, chemical and biological transformations, pharmacological and pharmacokinetic properties, and drug-likeness of SI are reviewed through a comprehensive literature survey, in order to provide support for its further research and applications. In general, SI is mainly distributed in Umbelliferae plants, and it is relatively stable to heat, acid, and oxygen, with good blood-brain barrier (BBB) permeability. Substantial studies have established reliable methods for the isolation, purification, and content determination of SI. Its pharmacological effects include analgesic, anti-inflammatory, antioxidant, anti-thrombotic, anti-tumor effects, alleviating ischemia-reperfusion injury, etc. Pharmacokinetic parameters indicate that its metabolic pathway is mainly phase Ⅱ metabolism, and it is rapidly absorbed in vivo and widely distributed in the kidneys, liver, and lungs.
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8.
QseB/QseC: a two-component system globally regulating bacterial behaviors.
Zhu, Y, Dou, Q, Du, L, Wang, Y
Trends in microbiology. 2023;(7):749-762
Abstract
QseB/QseC is a two-component system that is involved in the regulation of multiple bacterial behaviors by regulating quorum sensing, bacterial pathogenicity, and antibiotic resistance. Thus, QseB/QseC could provide a target for new antibiotic development. Recently, QseB/QseC has been found to confer survival advantages to environmental bacteria under stress conditions. The molecular mechanistic understanding of QseB/QseC has become an active area of research and revealed some emerging themes, including a deeper understanding of QseB/QseC regulation in different pathogens and environmental bacteria, the functional difference of QseB/QseC among species, and the possibility of analyzing QseB/QseC evolution. Here, we discuss the progression of QseB/QseC studies and describe several unresolved issues and future directions. Resolving these issues is among the challenges of future QseB/QseC studies.
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9.
The Role of Ferroptosis in Nervous System Disorders.
Du, L, Wu, Y, Fan, Z, Li, Y, Guo, X, Fang, Z, Zhang, X
Journal of integrative neuroscience. 2023;(1):19
Abstract
Ferroptosis is distinct from other apoptotic forms of programmed cell death and is characterized by the accumulation of iron and lipid peroxidation. Iron plays a crucial role in the oxidation of lipids via the Fenton reaction with oxygen. Hence, iron accumulation causes phospholipid peroxidation which induces ferroptosis. Moreover, detoxification by glutathione is disrupted during ferroptosis. A growing number of studies have implicated ferroptosis in nervous system disorders such as depression, neurodegenerative disease, stroke, traumatic brain injury, and sepsis-associated encephalopathy. This review summarizes the pathogenesis of ferroptosis and its relationship with various nervous system disorders.
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10.
Multiple Metabolites Derived from Mushrooms and Their Beneficial Effect on Alzheimer's Diseases.
Tong, Z, Chu, G, Wan, C, Wang, Q, Yang, J, Meng, Z, Du, L, Yang, J, Ma, H
Nutrients. 2023;(12)
Abstract
Mushrooms with edible and medicinal potential have received widespread attention because of their diverse biological functions, nutritional value, and delicious taste, which are closely related to their rich active components. To date, many bioactive substances have been identified and purified from mushrooms, including proteins, carbohydrates, phenols, and vitamins. More importantly, molecules derived from mushrooms show great potential to alleviate the pathological manifestations of Alzheimer's disease (AD), which seriously affects the health of elderly people. Compared with current therapeutic strategies aimed at symptomatic improvement, it is particularly important to identify natural products from resource-rich mushrooms that can modify the progression of AD. This review summarizes recent investigations of multiple constituents (carbohydrates, peptides, phenols, etc.) isolated from mushrooms to combat AD. In addition, the underlying molecular mechanisms of mushroom metabolites against AD are discussed. The various mechanisms involved in the antiAD activities of mushroom metabolites include antioxidant and anti-neuroinflammatory effects, apoptosis inhibition, and stimulation of neurite outgrowth, etc. This information will facilitate the application of mushroom-derived products in the treatment of AD. However, isolation of new metabolites from multiple types of mushrooms and further in vivo exploration of the molecular mechanisms underlying their antiAD effect are still required.