Catalogue Search | MBRL
Are you sure you want to remove the book from the shelf?
{{itemTitle}}
38
result(s) for
"Xie, Yi-Zi"
Sort by:
Motion-unrestricted dynamic electrocardiogram system utilizing imperceptible electronics
Electrocardiogram (ECG) plays a vital role in the prevention, diagnosis, and prognosis of cardiovascular diseases (CVDs). However, the lack of a user-friendly and accurate long-term dynamic electrocardiogram (DCG) device in motion has made it challenging to perform many daily cardiovascular risk screenings and assessments, such as sudden cardiac arrest, resulting in additional economic burdens on society. Here, we present a motion-unrestricted dynamic electrocardiogram (MU-DCG) system, which employs skin-conformal, imperceptible electronics for long-term, comfortable, and accurate 12-lead DCG monitoring. To facilitate assembly for use on the skin, the MU-DCG system features a pressure-activated flexible skin socket for stably soft-connecting the on-skin soft module and the off-skin stiff module during dynamic movements. Crucially, blinded cardiologist evaluations confirm minimal motion artifacts in MU-DCG-acquired ECG signals. Our results demonstrate that the MU-DCG system, with large-area, ultra-thin on-skin electrodes/leads, and an off-skin module, accomplishes anti-motion interference acquisition and in-situ analysis while retaining wearing imperceptibility.
Electrocardiogram is crucial for cardiovascular disease prevention, diagnosis, and prognosis. Here, the authors present a motion-unrestricted dynamic electrocardiogram system utilizing skin-conformal, imperceptible electronics for long-term, comfortable, and accurate 12-lead monitoring.
Journal Article
A Practical Strategy for Exploring the Pharmacological Mechanism of Luteolin Against COVID-19/Asthma Comorbidity: Findings of System Pharmacology and Bioinformatics Analysis
Asthma patients may increase their susceptibility to SARS-CoV-2 infection and the poor prognosis of coronavirus disease 2019 (COVID-19). However, anti-COVID-19/asthma comorbidity approaches are restricted on condition. Existing evidence indicates that luteolin has antiviral, anti-inflammatory, and immune regulation capabilities. We aimed to evaluate the possibility of luteolin evolving into an ideal drug and explore the underlying molecular mechanisms of luteolin against COVID-19/asthma comorbidity. We used system pharmacology and bioinformatics analysis to assess the physicochemical properties and biological activities of luteolin and further analyze the binding activities, targets, biological functions, and mechanisms of luteolin against COVID-19/asthma comorbidity. We found that luteolin may exert ideal physicochemical properties and bioactivity, and molecular docking analysis confirmed that luteolin performed effective binding activities in COVID-19/asthma comorbidity. Furthermore, a protein–protein interaction network of 538 common targets between drug and disease was constructed and 264 hub targets were obtained. Then, the top 6 hub targets of luteolin against COVID-19/asthma comorbidity were identified, namely, TP53, AKT1, ALB, IL-6, TNF, and VEGFA. Furthermore, the enrichment analysis suggested that luteolin may exert effects on virus defense, regulation of inflammation, cell growth and cell replication, and immune responses, reducing oxidative stress and regulating blood circulation through the Toll-like receptor; MAPK, TNF, AGE/RAGE, EGFR, ErbB, HIF-1, and PI3K–AKT signaling pathways; PD-L1 expression; and PD-1 checkpoint pathway in cancer. The possible “dangerous liaison” between COVID-19 and asthma is still a potential threat to world health. This research is the first to explore whether luteolin could evolve into a drug candidate for COVID-19/asthma comorbidity. This study indicated that luteolin with superior drug likeness and bioactivity has great potential to be used for treating COVID-19/asthma comorbidity, but the predicted results still need to be rigorously verified by experiments.
Journal Article
Modeling Kaempferol as a Potential Pharmacological Agent for COVID-19/PF Co-Occurrence Based on Bioinformatics and System Pharmacological Tools
Objective: People suffering from coronavirus disease 2019 (COVID-19) are prone to develop pulmonary fibrosis (PF), but there is currently no definitive treatment for COVID-19/PF co-occurrence. Kaempferol with promising antiviral and anti-fibrotic effects is expected to become a potential treatment for COVID-19 and PF comorbidities. Therefore, this study explored the targets and molecular mechanisms of kaempferol against COVID-19/PF co-occurrence by bioinformatics and network pharmacology. Methods: Various open-source databases and Venn Diagram tool were applied to confirm the targets of kaempferol against COVID-19/PF co-occurrence. Protein-protein interaction (PPI), MCODE, key transcription factors, tissue-specific enrichment, molecular docking, Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were used to clarify the influential molecular mechanisms of kaempferol against COVID-19 and PF comorbidities. Results: 290 targets and 203 transcription factors of kaempferol against COVID-19/PF co-occurrence were captured. Epidermal growth factor receptor (EGFR), proto-oncogene tyrosine-protein kinase SRC (SRC), mitogen-activated protein kinase 3 (MAPK3), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 8 (MAPK8), RAC-alpha serine/threonine-protein kinase (AKT1), transcription factor p65 (RELA) and phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit alpha isoform (PIK3CA) were identified as the most critical targets, and kaempferol showed effective binding activities with the above critical eight targets. Further, anti-COVID-19/PF co-occurrence effects of kaempferol were associated with the regulation of inflammation, oxidative stress, immunity, virus infection, cell growth process and metabolism. EGFR, interleukin 17 (IL-17), tumor necrosis factor (TNF), hypoxia inducible factor 1 (HIF-1), phosphoinositide 3-kinase/AKT serine/threonine kinase (PI3K/AKT) and Toll-like receptor signaling pathways were identified as the key anti-COVID-19/PF co-occurrence pathways. Conclusion: Kaempferol is a candidate treatment for COVID-19/PF co-occurrence. The underlying mechanisms may be related to the regulation of critical targets (EGFR, SRC, MAPK3, MAPK1, MAPK8, AKT1, RELA, PIK3CA and so on) and EGFR, IL-17, TNF, HIF-1, PI3K/AKT and Toll-like receptor signaling pathways. This study contributes to guiding development of new drugs for COVID-19 and PF comorbidities.
Journal Article
Uterine Natural Killer Cells: A Rising Star in Human Pregnancy Regulation
Uterine natural killer (uNK) cells are an immune subset located in the uterus. uNK cells have distinct tissue-specific characteristics compared to their counterparts in peripheral blood and lymphoid organs. Based on their location and the pregnancy status of the host, uNK cells are classified as endometrial NK (eNK) cells or decidua NK (dNK) cells. uNK cells are important in protecting the host from pathogen invasion and contribute to a series of physiological processes that affect successful pregnancy, including uterine spiral artery remodeling, fetal development, and immunity tolerance. Abnormal alterations in uNK cell numbers and/or impaired function may cause pregnancy complications, such as recurrent miscarriage, preeclampsia, or even infertility. In this review, we introduce recent advances in human uNK cell research under normal physiological or pathological conditions, and summarize their unique influences on the process of pregnancy complications or uterine diseases. Finally, we propose the potential clinical use of uNK cells as a novel cellular immunotherapeutic approach for reproductive disorders.
Journal Article
Super mitochondria-enriched extracellular vesicles enable enhanced mitochondria transfer
Mitochondria transfer is a spontaneous process that releases functional mitochondria to damaged cells via different mechanisms including extracellular vesicle containing mitochondria (EV-Mito) to restore mitochondrial functions. However, the limited EV-Mito yield makes it challenging to supply a sufficient quantity of functional mitochondria to damaged cells, hindering their application in mitochondrial diseases. Here, we show that the release of EV-Mito from mesenchymal stem cells (MSCs) is regulated by a calcium-dependent mechanism involving CD38 and IP3R signaling (CD38/IP3R/Ca
2+
pathway). Activating this pathway through our non-viral gene engineering approach generates super donor MSCs which produce Super-EV-Mito with a threefold increase in yield compared to Ctrl-EV-Mito from normal MSCs. Leber’s hereditary optic neuropathy (LHON), a classic mitochondrial disease caused by mtDNA mutations, is used as a proof-of-concept model. Super-EV-Mito rescues mtDNA defects and alleviates LHON-associated symptoms in LHON male mice. This strategy offers a promising avenue for enhancing mitochondria transfer efficiency and advancing its clinical application in mitochondrial disorders.
In mitochondria transplantation, the limited activity and yield of mitochondria constrain their clinical application for mitochondrial diseases. Here, authors develop a method for producing mitochondria-enriched extracellular vesicles, which offer high-quality, abundant mitochondrial material for transplantation.
Journal Article
Conjugated bile acids alleviate acute pancreatitis through inhibition of TGR5 and NLRP3 mediated inflammation
Introduction
Severe acute pancreatitis (SAP) is a crucial gastrointestinal disease characterized by systemic inflammatory responses and persistent multiple organ failure. The role of bile acids (BAs) in diverse inflammatory diseases is increasingly recognized as crucial, but the underlying role of BA conjugation remains elusive.
Objectives
Our study aim to investigate the potential role of conjugated bile acids in SAP and reveal the molecular mechanisms underlying its regulatory effects. We hypothesized that taurochenodeoxycholic acid (TCDCA) and glycochenodeoxycholic acid (GCDCA) could protect SAP through inhibiting the activation of NLRP3 inflammasomes via the TGR5 pathway in macrophages.
Methods
To test our hypothesis, we used BA-CoA: amino acid N-acyltransferase knockout (
Baat
−/−
) mice and established SAP mouse models using caerulein- and sodium taurocholate- induced. We utilized a range of methods, including pathology sections, qRT-PCR, immunofluorescence, Western blotting, and ELISA, to identify the mechanisms of regulation.
Results
BA-CoA: Amino acid N-acyltransferase knockout (
Baat
−/−
) mice significantly exacerbated pancreatitis by increasing pancreatic and systemic inflammatory responses and pancreatic damage in SAP mouse models. Moreover, the serum TCDCA levels in
Baat
−/−
mice were lower than those in wild-type (WT) mice with or without SAP, and GCDCA and TCDCA showed stronger anti-inflammatory effects than chenodeoxycholic acid (CDCA) in vitro. TCDCA treatment alleviated SAP in a Takeda G protein-coupled receptor 5 and
NOD-like receptor family, pyrin domain containing 3
—dependent manner in vivo. Reinforcing our conclusions from the mouse study, clinical SAP patients exhibited decreased serum content of conjugated BAs, especially GCDCA, which was inversely correlated with the severity of systemic inflammatory responses.
Conclusion
Conjugated bile acids significantly inhibit NLRP3 inflammasome activation by activating TGR5 pathway, thereby alleviating pancreatic immunopathology. The results provide new insights into the variability of clinical outcomes and paves the way for developing more effective therapeutic interventions for AP.
Journal Article
Curcumin Activates ROS Signaling to Promote Pyroptosis in Hepatocellular Carcinoma HepG2 Cells
Curcumin is a polyphenol that exerts a variety of pharmacological activities and plays an anti-cancer role in many cancer cells. It was recently reported that gasdermin E (GSDME) is involved in the progression of pyroptosis.
HepG2 cells were treated with various concentrations of curcumin and cell viability was examined using MTT assay, apoptosis was analysed using flow cytometry, reactive oxygen species (ROS) levels using dihydroethidium, LDH release using an LDH cytotoxicity assay, and protein expression using western blot.
Curcumin increased the expression of the GSDME N-terminus and proteins involved in pyrolysis, promoted HspG2 cell pyrolysis and increased intracellular ROS levels. Moreover, inhibition of the production of intracellular ROS with n-acetylcysteine (NAC) improved the degree of apoptosis and pyrolysis induced by curcumin.
Curcumin induces HspG2 cell death by increasing apoptosis and pyroptosis, and ROS play a key role in this process. This study improves our understanding of the potential anti-cancer properties of curcumin in liver cancer.
Journal Article
Subpleural injection of gelatin sponge particles to reduce pneumothorax incidence in CT-guided lung biopsies: a retrospective single-center case-control study
Background
To evaluate the efficacy and safety of track sealing using subpleural injection of gelatin sponge particles in reducing the incidence of pneumothorax after percutaneous CT-guided lung biopsy.
Methods
This study conducted a retrospective analysis of 1,026 patients who underwent CT-guided lung biopsy at our center from January 2022 to July 2024. After propensity score matching (PSM) to minimize the impact of confounding variables like smoke, lesion diameter, and tract length, 338 patients were ultimately included and assigned to the sealant group (169 patients) or the non-sealing group (169 patients) according to whether using the gelatin sponge particles sealing after needle withdraw to the subpleural area. Clinical and operative characteristics data were collated from electronic medical records (EMR) and Picture Archiving and Communication Systems (PACS). A multivariable logistic regression analysis was conducted to identify predictors of pneumothorax.
Results
In the sealing group, the incidence of pneumothorax was 14.8%, whereas it was significantly higher in the non-sealing group at 23.7% (
p
< 0.05). There was no significant difference in the chest tube placement rates of 3% and 1.8% (
p
= 0.723). Importantly, no significant complications, such as air embolism, were observed in either group. A multivariate logistic regression analysis, using a propensity score-matched cohort, identified patient emphysema (OR = 2.35 [1.22–4.51],
p
= 0.01) and the tract length (OR = 1.25 [1.01–1.55],
p
= 0.042) as significant risk factors for pneumothorax. Furthermore, gelatin sponge particle needle-tract sealing demonstrated a marked and statistically significant reduction in the risk of pneumothorax (OR = 0.5 [0.27–0.91],
p
= 0.024), highlighting the distinct advantages and clinical value of this treatment in preventing such complications.
Conclusions
The gelatin sponge particle subpleural sealing technique can effectively reduce the incidence of pneumothorax in patients undergoing percutaneous CT-guided lung biopsy.
Journal Article
Mitochondria-targeted gene delivery using fluorinated lipid nanoparticles to alleviate Leber’s hereditary optic neuropathy
Mutations in mitochondrial DNA (mtDNA) lead to various mitochondrial diseases for which no cure is currently available. Despite the promising potential of mtDNA correction to treat these disorders, the double mitochondrial membranes have proven to be a tough barrier to overcome. Here, we develop fluorinated lipid nanoparticles with a mitochondrial targeting sequence (F-M-LNP) to overcome the mitochondrial barrier by virtue of their high affinity for mitochondrial membranes, thereby effectively introducing gene into mitochondria. Through the rational design of ionizable lipid structures, we synthesize 16 lipid nanoparticles (LNPs) with varying degrees of fluorination and investigate the key structural features required for efficient mitochondria-targeted gene delivery. As fluorinated ionizable lipid-mediated mitochondrial transport is independent of mitochondrial membrane potential (MMP), F-M-LNPs deliver gene to mitochondria under pathological conditions where MMP is impaired, resulting in a 3.8-fold increase in functional protein expression compared to non-fluorinated LNPs. In a male mouse model of genetically induced mitochondrial disease, F-M-LNP demonstrate functional complementation of mutant mtDNA, alleviating disease symptoms. Together, our results show that modifying vectors with fluorinated groups offers valuable tools for correcting mitochondrial genome defects.
The mitochondrial membranes present a formidable barrier to the delivery of exogenous genes. Here, the authors report on the development of fluorinated lipid nanoparticles to efficiently introduce therapeutic genes into mitochondria, for the correction of mitochondrial genomic defects.
Journal Article