Feng Wang’s research while affiliated with Chinese Academy of Sciences and other places

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Publications (595)


Size-Dependent Dynamic Response Analysis of Magneto-Electro-Elastic Nanobeams Based on Nonlocal Modified Couple Stress Theory
  • Article

March 2025

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4 Reads

Journal of Vibration Engineering & Technologies

Yang Zhou

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Yu-fang Zheng

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Feng Wang

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Chang-ping Chen

In the context of rapid nanotechnology advancements, size effects have become key in determining material performance. In order to better investigate the impact of size effects on nanostructures, a new nonlocal modified couple stress (NL-MCS) model developed for magneto-electro-elastic (MEE) nanobeams is introduced in this research. This model comprehensively incorporates size-dependent effects, prominently reflecting the softening characteristics introduced by the nonlocal elasticity theory (NL), while also accounting for the influence of modified couple stress (MCS) on hardening. The model incorporates von Karman’s geometric nonlinearity theory, Reddy’s third-order shear deformation theory and Maxwell’s equations. The objective of this paper is to analyze the dynamic response behavior of MEE nanostructures, providing a theoretical foundation for the design and mechanical response of MEE nanostructures. The Galerkin method is employed to process the dynamic model of MEE nanobeams, followed by iterative solution of the processed model using the Newmark method. Additionally, quadratic extrapolation is utilized to enhance the convergence rate of the iterative process. A comprehensive analysis of the influences of material length scale parameter, nonlocal parameters, Winkler–Pasternak coefficients, aspect ratio, volume fraction of materials, applied magnetic potential and applied voltage on the nonlinear dynamic response of MEE nanobeams are conducted.



Characterization of Heterogeneity in SS-USCs and RS-USCs. A Experimental design and analysis of extracting USCs from human urine samples. B Heatmap displaying the differentially expressed genes (DEGs) between SS-USCs and RS-USCs groups (n = 3) based on Bulk RNA-seq data. C GO analysis of DEGs from Bulk RNA-seq, showing enrichment in 11 biological processes. D Score analysis based on characteristic gene sets of SS-USCs/RS-USCs, dividing them into three major clusters (C1, C2, and C3). E scRNA-seq heatmap: Top 10 DEGs in subgroups C1/C3. F scRNA-seq Bar plots performing GO and KEGG analysis on DEGs, showing enrichment in 10 biological processes for SS-USCs and RS-USCs respectively
SS-USCs inhibit ferroptosis to alleviate SHP-HR. A Diagram illustrating the SHP-HR experimental design. B Oil Red O staining showing lipid degeneration in HL7702 cells subjected to the S-HL7702 treatment. C Flow cytometry analysis comparing cell death rates among different groups (Control, HR, RS-USCs, and SS-USCs), with quantification (n = 3). D Cell viability assessed by the CCK-8 assay (n = 3). E Lipid-ROS levels measured using C11-BODIPY staining (n = 3). F GPX4 levels in each group, normalized to β-actin (n = 3). G, H Measurements of Fe2 + and MDA levels in cells across all groups (n = 3), *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001
SS-USCs reduce ferroptosis, alleviating IRI in rat and mouse livers with severe steatosis. A Experimental protocol for creating a rat model of severe fatty liver transplantation. B Experimental protocol for the mouse model of severe fatty liver IRI. C, D Oil Red O staining of severe fatty liver tissues in both rats and mice. E, F H&E and TUNEL staining of liver tissues from different treatment groups (Sham, PBS, RS-USCs, and SS-USCs), with necrotic regions highlighted (n = 5). G, H Measurement of serum ALT and AST levels in both rat and mouse groups (n = 5). (I, J) Quantification of Fe²⁺ and MDA levels in rat liver tissues (n = 5). (K, L) Quantification of Fe2 + and MDA levels in mouse liver tissues (n = 5). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001
SS-USCs inhibit ferroptosis to alleviate SHP-HR through the utilization of Exosomes. A Flow cytometry analysis of cell death rates; the exosome inhibitor GW4869 significantly attenuates the protective effect of SS-USCs on cell damage (n = 3). B Elevated levels of Lipid ROS after treatment of SS-USCs with GW4869. C Transmission electron microscopy image showing exosomes isolated from USCs conditioned medium (scale bar = 200 nm).D Analysis of size distribution of USCs-Exo, revealing an average diameter of 102.4 ± 9.8 nm. E Western blot validation of exosome markers CD9, CD63, CD81, and HSP70, with conditioned medium (CM) as the control group. F Cell viability measured by CCK-8 assay (n = 3). G Fluorescence images showing S-HL7702 cells uptake CM-DiI-labeled (red) exosomes. H Flow cytometry analysis of cell death rates across different treatment groups (HR, RS-USCs-Exo, SS-USCs-Exo) (n = 3). I CCK-8 assay measuring cell viability (n = 3). J Elevated Fe²⁺ levels after treating SS-USCs with GW4869. K Lipid ROS levels (C11-BODIPY) detection in various treatment groups (HR, RS-USCs-Exo, SS-USCs-Exo) (n = 3). L, M Measurement of MDA and Fe2 + levels in cells from each group (n = 3). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001
SS-USCs inhibit ferroptosis by utilizing exosomes in rat donor liver with severe steatosis and mouse liver with severe steatosis. A, B H&E and TUNEL staining of liver tissues from various treatment groups (Sham, PBS, RS-USCs-Exo, SS-USCs-Exo) in both rat and mouse models, highlighting necrotic areas (n = 5). C, D Measurement of serum ALT and AST levels in rat and mouse subjects (n = 5). E, F Quantification of Fe2 + and MDA levels in liver tissues of rat groups (n = 5). G, H Analysis of Fe2 + and MDA levels in mouse liver tissues (n = 5). I, J GPX4 levels in liver tissues from rats and mice, normalized to β-actin (n = 3). K, L Immunohistochemical staining to display GPX4 levels across treatment groups (n = 5). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001

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Human spindle-shaped urine-derived stem cell exosomes alleviate severe fatty liver ischemia–reperfusion injury by inhibiting ferroptosis via GPX4
  • Article
  • Full-text available

February 2025

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5 Reads

Stem Cell Research & Therapy

Background Severe hepatic steatosis can exacerbate Ischemia–reperfusion injury (IRI), potentially leading to early graft dysfunction and primary non-function. In this study, we investigated the heterogeneity of different subpopulations of Urine-derived stem cells (USCs) to explore the most suitable cell subtype for treating severe steatotic liver IRI. Methods This study utilized scRNA-seq and Bulk RNA-seq to investigate the transcriptional heterogeneity between Spindle-shaped USCs (SS-USCs) and Rice-shaped USCs (RS-USCs). Additionally, rat fatty Liver transplantation (LT) model, mouse fatty liver IRI model, and Steatotic Hepatocyte Hypoxia-Reoxygenation (SHP-HR) model were constructed. Extracellular vesicles derived from SS-USCs and RS-USCs were isolated and subjected to mass spectrometry analysis. The therapeutic effects of Spindle-shaped USCs Exosomes (SS-USCs-Exo) and Rice-shaped USCs Exosomes (RS-USCs-Exo) were explored, elucidating their potential mechanisms in inhibiting ferroptosis and alleviating IRI. Results Multiple omics analyses confirmed that SS-USCs possess strong tissue repair and antioxidant capabilities, while RS-USCs have the potential to differentiate towards specific directions such as the kidney, nervous system, and skeletal system, particularly showing great application potential in renal system reconstruction. Further experiments demonstrated in vivo and in vitro models confirming that SS-USCs and SS-USCs-Exo significantly inhibit ferroptosis and alleviate severe fatty liver IRI, whereas the effects of RS-USCs/RS-USCs-Exo are less pronounced. Analysis comparing the proteomic differences between SS-USCs-Exo and RS-USCs-Exo revealed that SS-USCs-Exo primarily inhibit ferroptosis and improve cellular viability by secreting exosomes containing Glutathione Peroxidase 4 (GPX4) protein. This highlights the most suitable cell subtype for treating severe fatty liver IRI. Conclusions SS-USCs possess strong tissue repair and antioxidant capabilities, primarily alleviating ferroptosis in the donor liver of fatty liver through the presence of GPX4 protein in their exosomes. This highlights SS-USCs as the most appropriate cell subtype for treating severe fatty liver IRI.

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ECs are the most significant contributors to AD among all cell subpopulations in the brain. (A) UMAP plot of all cells in the GSE157827 dataset, highlighting clustering into 16 subtypes based on transcriptomic profiles, with numeric labels in various colors representing individual clusters. (B) UMAP plot annotated with six major cell types: oligodendrocytes, excitatory neurons, astrocytes, inhibitory neurons, microglia, and ECs. The spatial distribution highlights the clustering of distinct cell populations, reflecting their transcriptional heterogeneity. (C) Stacked bar plot displaying the percentage composition of each cell type across samples, revealing variability in cell type proportions among individuals. (D) Bar plot of fold change scores (FCscore), quantifying the contribution of each major cell type to AD.
Identification of EC−related key genes for AD through machine learning. (A) Coefficient values of the 14 characteristic genes of AD identified by LASSO regression. (B) Relative importance of top 10-ranking genes identified by the random forest algorithm. (C) Venn diagram displaying the overlap of three key genes (EIF1, HSPA1B, and KCTD12) identified by LASSO regression and random forest analysis. (D) Dot plot showing the expression levels of EIF1, HSPA1B, and KCTD12 across six major cell types. (E) UMAP plots illustrating the percentage of cells expressing the genes EIF1, HSPA1B, and KCTD12 within different cell types, respectively. It should be noted that KCTD12 exhibited its highest expression in microglial cells rather than ECs. Consequently, EIF1 and HSPA1B were selected for further investigation in the present study as pivotal genes associated with AD.
Transcriptional regulation and pathway enrichment of EC−related key genes in AD. (A) Predicted motifs associated with the regulation of EIF1 and HSPA1B based on motif enrichment analysis. (B) Gene set enrichment analysis (GSEA) indicates that EIF1 is associated with the HIF-1 signaling pathway, IL-17 signaling pathway, and spliceosome. (C) GSEA indicates that HSPA1B is linked to the Notch signaling pathway, p53 signaling pathway, and TNF signaling pathway. (D) Gene set variation analysis (GSVA) of pathways associated with EIF1. GSVA scores are compared for high versus low expression groups of EIF1. High expression of EIF1 correlates with pathways including DNA repair, PI3K-Akt-mTOR signaling, and protein secretion. (E) GSVA of pathways associated with HSPA1B. GSVA scores are compared for high versus low expression groups of HSPA1B. High expression of HSPA1B is associated with TGF-β signaling, PI3K-Akt-mTOR signaling, and the p53 pathway.
Immune infiltration analysis highlights the interactions of EC−related key genes with peripheral immunoinflammatory processes in AD. (A) Heatmap depicting the relative abundance of 29 immune cell types across different groups in our own dataset containing 7 NC subjects and 23 AD clinical continuum patients (8 patients with MCI, 7 patients with mild ADD, and 8 patients with moderate ADD). (B) Boxplot of immune cell infiltration scores, showing differences between NC subjects and AD clinical continuum patients. (C) Correlation between endothelial EIF1 and HSPA1B expression and immune infiltration markers. (D) Dot plots showing the correlation of EIF1 and HSPA1B with various immune factors, including chemokines, immunosuppressive factors, immunostimulatory factors, MHCs, and receptors (data downloaded from TISIDB database). * p < 0.05; ** p < 0.01, ns = not significant.
Dynamic expression patterns of EIF1 and HSPA1B in peripheral blood and their association with cognitive functions of AD clinical continuum patients. (A) Boxplots displaying the dynamic alteration of EIF1 in the peripheral blood across different AD stages. (B) Boxplots displaying the dynamic alteration of HSPA1B in the peripheral blood across different AD stages. (C) Scatter plot showing the correlation between EIF1 expression and MoCA or CDR−SB scores in AD clinical continuum patients. * p < 0.05; ** p < 0.01.
The Endothelial Cell-Related Genes EIF1 and HSPA1B Contribute to the Pathogenesis of Alzheimer’s Disease by Modulating Peripheral Immunoinflammatory Responses

February 2025

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8 Reads

Background: Emerging evidence suggests that peripheral immunoinflammatory responses contribute to Alzheimer’s disease (AD) pathogenesis, and endothelial cells (ECs) are involved in these responses. Nevertheless, the potential molecular mechanisms and signaling pathways by which ECs modulate peripheral immunoinflammatory responses and thus contribute to AD pathogenesis are not fully understood. Methods: The single-cell RNA sequencing dataset GSE157827 was analyzed, and AD key genes were screened using LASSO regression and random forest algorithms. Functional enrichment analyses of these AD key genes were conducted using gene set enrichment analysis (GSEA) and gene set variation analysis. Immune cell infiltration analyses for AD key genes were performed using single-sample GSEA, and their correlations with immunoinflammatory factors were assessed using the TISIDB database. Peripheral blood RNA sequencing data from our cohort were utilized to validate the expression patterns of EC-related AD key genes in peripheral blood and to investigate their association with cognition. Results: ECs are the most significant contributors to AD among all brain cell subpopulations. For the first time, the EC-related genes EIF1 and HSPA1B were identified as key genes associated with AD progression. These two EC-related key genes may participate in AD pathogenesis by modulating peripheral immunoinflammatory responses. The levels of EIF1 and HSPA1B were significantly altered in the peripheral blood during AD progression, and EIF1 levels correlated with cognitive functions in AD clinical continuum patients. Conclusions: These findings underscore the critical roles of the EC-related genes EIF1 and HSPA1B in AD pathogenesis and their potential as biomarkers for this disease.



Potential mechanisms between the oral microbiome and brain. Created with BioGDP.com.³⁰ (A) Oral microbiota and pathogens invasion through the oral mucosal barrier; (B) immune‐inflammation response within the host caused by bacterial invasion; (C) cytokines traversed through the brain‐blood barrier activate neuroinflammation; (D) direct invasion of the pathogens through trigeminal nerves; (E) neurotransmission process in the pathogenesis of central nervous system diseases within the brain; (F) HPA axis. 5‐HT, 5‐hydroxy tryptamine; ACTH, adrenocor ticotropic hormore; GABA, gamma‐aminobutyric acid; HPA, hypothalamic‐pituitary‐adrenal; IL, interleukin; Phe, phenylalanine; TNF‐α, tumor necrosis factor‐α; Trp, tryptophan; Tyr, tyrosine.
Oral microbiota and central nervous system diseases: A review

February 2025

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28 Reads

Oral microbiota is the second largest microbial colony in the body and forms a complex ecological community that influences oral and brain health. Impaired homeostasis of the oral microbiota can lead to pathological changes, resulting in central nervous system (CNS) diseases. However, the mechanisms and clinical value of how the oral microbiome influences the brain remain unclear. This review summarizes recent clinical findings on the role of the oral microbiota in CNS diseases and proposes potential approaches to understand the way the oral microbiota and brain communicate. We propose three underlying patterns involving neuroinflammation, neuroendocrine regulation, and CNS signaling between oral microbiota and CNS diseases. We also summarize the clinical characteristics and potential utilization of the oral microbiota in ischemic stroke, Alzheimer's and Parkinson's disease, intracranial aneurysms, and mental disorders. Although the current findings are preliminary and clinical evidence is incomplete, oral microbiota is a potential biomarker for the clinical diagnosis and treatment of CNS diseases.


Trends in the Burden of Epilepsy in China from 1990 to 2021 and Its Forecast until 2044: Based on the 2021 Global Burden of Disease Study

February 2025

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10 Reads

QJM: monthly journal of the Association of Physicians

Background Epilepsy is one of the most prevalent neurological disorders, but no updated analysis of its burden in China. Aims This study provides the most up-to-date, comprehensive analysis of temporal trends and predicts future trends of idiopathic epilepsy in China. Design Secondary analysis based on the Global Burden of Disease (GBD). Methods GBD 2021 data were analyzed to estimate the incidence, prevalence, mortality, and Disability-Adjusted Life Years (DALYs) of epilepsy in China across different genders, age groups, and years. Joinpoint regression and decomposition analysis assessed temporal changes and the contributions of aging, population growth, and epidemiological changes to disease trends. The Bayesian Age-Period-Cohort (BAPC) model was used to predict age-standardized rates (ASRs) per 100,000 individuals until 2044. Results In 2021, the ASRs of incidence, prevalence, deaths, and DALYs for epilepsy in China were 28.2 (95% uncertainty interval [UI]: 19.0–37.9), 214.7 (150.1–278.6), 0.8 (0.7–1.0), and 101.4 (72.5–139.4) per 100,000 population, respectively. The incidence and prevalence rates were 26.1% and 13.4% higher than those in 1990, while deaths and DALYs decreased by 56.6% and 43.2%, respectively, compared to 1990. The highest burden was seen in the youngest and older adults, with men more affected than women. Predictions indicate rising incidence and prevalence rates by 2044, alongside declining mortality and disability rates. Conclusion Epilepsy poses a significant health burden in China, with increasing incidence and prevalence from 1990 to 2021, and projections indicating a continued rise through 2044. The disease burden also varies across genders, age groups, and time periods.


Cortical structural degeneration and functional network connectivity changes in patients with subcortical vascular cognitive impairment

Neuroradiology

Purpose To explore the structural basis of functional network connectivity (FNC) changes and early cortical degenerative patterns in subcortical vascular cognitive impairment (SVCI). Methods We prospectively included SVCI cases and healthy controls (HCs). FNC alterations were evaluated using group-independent component analysis of resting-state functional MRI data. Cortical microstructural and macrostructural alterations were assessed using gray matter-based spatial statistics analysis with neurite orientation dispersion and density imaging and cortical thickness analysis with FreeSurfer software on T1-weighted images, respectively. Spearman correlation analyses were performed to assess relationships between FNC alterations and cortical microstructural/macrostructural alterations and between FNC, cortical thickness, or neurite density index (NDI)/orientation dispersion index (ODI) alterations and cognitive performance. Results Forty-six SVCI patients and 73 HCs were recruited. FNC analysis showed lower network connectivity between the visual network (VN) and sensorimotor network (SMN) in SVCI, positively correlated with information processing speed (p=0.008) and negatively with summary SVD score (p = 0.037). Cortical microstructural analyses exhibited a lower NDI, mainly in the VN and default mode network (DMN) areas (PFWE < 0.05, cluster > 100 voxels), and lower ODI, mainly in the SMN and DMN areas (PFWE < 0.05, cluster > 100 voxels) in SVCI, both of which were related to cognitive function (p < 0.05). However, cortical thickness did not differ between groups. Lower NDI in the lateral occipital cortex was linked to lower VN-SMN connectivity in SVCI (p = 0.002). Conclusion Cortical microstructural alterations may serve as the basis for FNC changes in SVCI Graphical abstract



Optimizing photothermal CO2 reduction through integrated band-division utilization and thermal management structure

February 2025

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22 Reads

Solar-driven photothermal catalytic CO2 conversion into fuels offers a promising approach to reducing fossil fuel dependence. To enhance the efficiency of photothermal CO2 reduction, photothermal catalyst design must not only sustain the high temperatures required for the reaction but also effectively utilize the entire solar spectrum. In this study, we present a novel photothermal catalyst architecture BiVO4/Bi/BiOCl that surpasses traditional designs by integrating plasmonic metal Bi as the “hot spot” and BiOCl as the thermal insulation layer on the outermost part. This structure realizes thermal management, contributing to maintaining the high temperatures required for the reaction. The BiVO4/Bi/BiOCl multi-component system synergistically absorbs the full solar light spectrum and achieves band-division utilization: short- and mid-wavelengths drive reduction and oxidation reactions, respectively, while long-wavelengths induce the photothermal effect. The BiVO4/Bi/BiOCl catalyst demonstrates high-efficiency CO2 conversion performance in an outdoor concentrating system, achieving a CO production rate of 9.5 μmol/h. This work presents a design strategy for functional photothermal catalysts, making them viable candidates for industrial-scale CO2 conversion processes.


Citations (28)


... Under fullspectrum irradiation, the CO production rate of CuInS 2 reaches 19.9 μmol·g −1 h −1 , which is more than seven times that under UV−visible light irradiation alone. 32 Despite these advancements, In-based sulfides still face some challenges in the photocatalytic CO 2 reduction process. The regulation mechanism of reaction pathways and long-term stability (>200 h) remain bottlenecks for industrial applications. ...

Reference:

Recent Advances of Indium-Based Sulfides in Photocatalytic CO 2 Reduction
Anti-Site Defect-Induced Cascaded Sub-Band Transition in CuInS2 Enables Infrared Light-Driven CO2 Reduction
  • Citing Article
  • December 2024

ACS Nano

... However, The success of M7824 in preclinical studies but failure in both a phase II clinical trial (NCT02699515) for advanced biliary tract cancer and a phase III trial (NCT03631706) for non-small cell lung cancer (NSCLC) indicates the dilemma of transitioning from animal models to clinical trials. Interestingly, SHR-1701, a bifunctional protein targeting PD-L1 and TGF-β, was reported to exhibit a manageable safety profile and potent antitumor activity in unresectable metastatic colorectal cancer [69], implying a significance difference between human and animal TGF-β signal pathway. Moreover, since TGF-β signal plays an important role from embryonic development to the maintenance of immune homeostasis [70], systemic TGF-β deficiency caused by widespread inhibition may lead to the disturbance of normal physiological processes [71]. ...

Addition of SHR-1701 to first-line capecitabine and oxaliplatin (XELOX) plus bevacizumab for unresectable metastatic colorectal cancer

Signal Transduction and Targeted Therapy

... In The Lancet, Jianmin Liu and colleagues report results of the multicentre PROTECT-MT trial investigating the effectiveness of using a balloon guide catheter during endovascular thrombectomy for patients with acute ischaemic stroke due to large vessel occlusion of the anterior circulation within 24 h of symptom onset. 9 Based on the prospective, randomised, open-label, and blinded-endpoint design, 329 participants (median age 69 years [IQR 59-76]; 201 [61%] were male and 128 [39%] female) were randomly assigned to the balloon guide catheter group or conventional guide catheter group at 28 hospitals in China between Feb 7 and Nov 13, 2023. The primary outcome was functional recovery based on the modified Rankin scale at 90 days. ...

Balloon guide catheters for endovascular thrombectomy in patients with acute ischaemic stroke due to large-vessel occlusion in China (PROTECT-MT): a multicentre, open-label, blinded-endpoint, randomised controlled trial
  • Citing Article
  • November 2024

The Lancet

... By producing secondary beams at F0 using projectile fragmentation method, and then following that with the separation and transportation of nuclei of interest via beam line from F0 to F2, a series of experiments has been carried out at ETF, such as knock-out reaction studies (e.g., Ref. [10]), production cross section measurements (e.g., Ref. [11]), charge-changing cross section (CCCS) measurements (e.g., Refs. [12,13]), and charge radius investigations [14] based on the recently discovered robust correlation between CCCS and separation energies [15]. Since the beam line from F0 to F2 has a limited separation capability and relatively short flight path ( 26 m), the aforementioned experiments were mainly dedicated to study the p-or sd-shell nuclei by employing the light primary beams (such as 18 O and 40 Ar). ...

Single-proton removal reaction in the IQMD+GEMINI model benchmarked by elemental fragmentation cross sections of 29−33Si on carbon at ∼230 MeV/nucleon

Physics Letters B

... Additionally, the moderate decay half-life ensures favorable radiation safety, balancing effective imaging with minimized internal radiation exposure to patients. Importantly, previous studies have reported that 64 Cu can be selectively accumulated in the tumor with the assistance of copper transporters and chaperone proteins, such as copper transporter 1 (hCTR1) [21,22]. In addition, the abundant coordination chemistry of copper allows it to form stable complexes with nanoparticles or other delivery vehicles. ...

Copper-64 Based PET-Radiopharmaceuticals: Ways to Clinical Translational
  • Citing Article
  • November 2024

Seminars in Nuclear Medicine

... In addition to their direct effects on pathogenic microorganisms, various beneficial rhizosphere microbes can enhance the defense mechanisms of the above-ground portions of plants, thereby reducing the incidence of diseases [11]. Concurrently, biocontrol agents can augment the abundance of beneficial bacteria within phyllosphere microbial communities and mitigate disease by displacing pathogenic bacterial niches [12,13]. Phage biocontrol utilizing plant pathogen-specific viruses to manipulate phyllosphere microbiota presents a potentially effective approach for safeguarding plants against diseases. ...

Phyllospheric microbial community structure and carbon source metabolism function in tobacco wildfire disease

... The raw scRNA sequencing data were processed using the "Seurat" package (version 4.3.0.1) and analyzed with the "DoubletFinder" package (version 2.0.3) to identify potential doublets [20]. Cells were excluded if they had fewer than 300 or more than 6000 genes; fewer than 500 total molecules (nCount_RNA); more than 100,000 total molecules; more than 20% of their genes; or with over 5% mitochondrial gene expression [21,22]. ...

Single-cell mapping of peripheral blood mononuclear cells reveals key transcriptomic changes favoring coronary artery lesion in IVIG-resistant Kawasaki disease

Heliyon

... Folic acid (FA) is an essential vitamin that participates in a variety of biological functions in cells and acts as a coenzyme and substrate in many physiological processes [1][2][3][4][5]. Whereas, deficiency or excess of FA can result in harmful consequences such as leukopenia, lowered cysteine levels, megaloblastic anemia, and congenital fetal defects [6][7][8]. ...

Maternal folic acid over-supplementation impairs cardiac function in mice offspring by inhibiting SOD1 expression

Cardiovascular Research

... The electrochemical CO 2 reduction reaction (CO 2 RR) conversion into value-added chemicals or fuels offers a promising strategy to mitigate the excessive burning of fossil fuels and the greenhouse effect, especially driven by renewable energy. [1][2][3] Among the various products, the energy-intensive formic acid/formate derived from the CO 2 RR receives remarkable attention because of their promising potential as fundamental raw material for chemical feedstock. [4][5][6][7][8] To meet the technoeconomic analysis of the CO 2 RR to formic acid/formate, developing highly-active electrocatalysts with high activity/selectivity and substantial economic DOI: 10.1002/adfm.202420177 ...

Stabilized High‐Valent Indium for Promoted Formate Production from Electrochemical CO2 Reduction

... In contrast, the immunological defense functions of CD8 + T RM have been linked to graft tolerance during liver transplantation. These cells are characterized by distinct expression profiles of tissue-residency markers, immune checkpoints, cytotoxic markers, and proliferative markers, along with high expression levels of transcription factors, including EOMES and RUNX3 [8]. Zhu et al. also explored the pathogenic role of CD8 + T RM in primary biliary cholangitis, a cholestatic autoimmune liver disease, underscoring their involvement in autoimmunity against self-antigens [9]. ...

Single cell RNA-sequencing delineates CD8 + tissue resident memory T cells maintaining rejection in liver transplantation

Theranostics