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A review on traditional Chinese medicine natural products and acupuncture intervention for Alzheimer's disease based on the neuroinflammatory.
Chen, Z, Wang, X, Du, S, Liu, Q, Xu, Z, Guo, Y, Lin, X
Chinese medicine. 2024;(1):35
Abstract
Alzheimer's disease (AD) is a neurodegenerative disease with insidious onset and progressive development. It is clinically characterized by cognitive impairment, memory impairment and behavioral change. Chinese herbal medicine and acupuncture are important components of traditional Chinese medicine (TCM), and are commonly used in clinical treatment of AD. This paper systematically summarizes the research progress of traditional Chinese medicine natural products and acupuncture treatment of AD, which combined with existing clinical and preclinical evidence, based on a comprehensive review of neuroinflammation, and discusses the efficacy and potential mechanisms of traditional Chinese medicine natural products and acupuncture treatment of AD. Resveratrol, curcumin, kaempferol and other Chinese herbal medicine components can significantly inhibit the neuroinflammation of AD in vivo and in vitro, and are candidates for the treatment of AD. Acupuncture can alleviate the memory and cognitive impairment of AD by improving neuroinflammation, synaptic plasticity, nerve cell apoptosis and reducing the production and aggregation of amyloid β protein (Aβ) in the brain. It has the characteristics of early, safe, effective and benign bidirectional adjustment. The purpose of this paper is to provide a basis for improving the clinical strategies of TCM for the treatment of AD.
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Emerging Contaminants: An Emerging Risk Factor for Diabetes Mellitus.
Niu, H, Xu, M, Tu, P, Xu, Y, Li, X, Xing, M, Chen, Z, Wang, X, Lou, X, Wu, L, et al
Toxics. 2024;(1)
Abstract
Emerging contaminants have been increasingly recognized as critical determinants in global public health outcomes. However, the intricate relationship between these contaminants and glucose metabolism remains to be fully elucidated. The paucity of comprehensive clinical data, coupled with the need for in-depth mechanistic investigations, underscores the urgency to decipher the precise molecular and cellular pathways through which these contaminants potentially mediate the initiation and progression of diabetes mellitus. A profound understanding of the epidemiological impact of these emerging contaminants, as well as the elucidation of the underlying mechanistic pathways, is indispensable for the formulation of evidence-based policy and preventive interventions. This review systematically aggregates contemporary findings from epidemiological investigations and delves into the mechanistic correlates that tether exposure to emerging contaminants, including endocrine disruptors, perfluorinated compounds, microplastics, and antibiotics, to glycemic dysregulation. A nuanced exploration is undertaken focusing on potential dietary sources and the consequential role of the gut microbiome in their toxic effects. This review endeavors to provide a foundational reference for future investigations into the complex interplay between emerging contaminants and diabetes mellitus.
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Experimental research on compressive strength deterioration of coal seam floor sandstone under the action of acidic mine drainage.
Han, W, Chen, Z, Liu, H, Zheng, X, Wu, J, Yuan, Q
Scientific reports. 2024;(1):4593
Abstract
In sulphur-coal symbiotic coal seams, after the mining of sulphide iron ore, when the coal resources are mined, the mine water accumulated in the roadway mining area will have a certain impact on the stability of the surrounding rock of the coal seam roadway. Taking the floor sandstone of sulfur coal symbiotic coal seam as the research object, the roof fissure water with pH values of 7.48, 4.81 and 2.62 was used as the experimental solution. 10 experimental schemes were designed to measure the compressive strength of the samples under the action of AMD, and the hydrochemical analysis of AMD was conducted. The pore structures of the samples before and after the action of AMD were analyzed. Based on the hydrochemistry and pore structure, the deterioration mechanism of compressive strength of the coal seam floor sandstone under the action of AMD was explained. The results indicated that the compressive strength of the samples decreased with the increasing action time of AMD. The compressive strength decreased with the increment of the porosity. The concentration of H+ ion in AMD was relatively small. Na2O in albite dissolved and reacted with water, leading to an increase in the concentration of Na+ ion. Soluble substances such as MgCl2 and CaSO4 in the pore structure dissolved, leading to an increase in the concentration of Ca2+ and Mg2+ ions. The dissolution of soluble substances and the physical-chemical reactions between solutions and minerals were the essential causes of the continuous deterioration of the compressive strength of the coal seam floor sandstone. The results of this study can provide a theoretical basis for the deterioration of the mechanical properties of the peripheral rock in the roadway of the sulphur coal seam, and can also provide a certain engineering reference for the sulphur coal seam roadway.
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Curcumin suppresses metastasis of triple-negative breast cancer cells by modulating EMT signaling pathways: An integrated study of bioinformatics analysis.
Chen, Z, Lu, P, Li, M, Zhang, Q, He, T, Gan, L
Medicine. 2024;(8):e37264
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Abstract
This study aimed to use bioinformatics approaches for predicting the anticancer mechanisms of curcumin on triple-negative breast cancer (TNBC) and to verify these predictions through in vitro experiments. Initially, the Cell Counting Kit-8 (CCK8) assay was employed to rigorously investigate the influence of curcumin on the proliferative capacity of TNBC cells. Subsequently, flow cytometry was employed to meticulously assess the impact of curcumin on cellular apoptosis and the cell cycle regulation. Transwell assays were employed to meticulously evaluate the effect of curcumin on the motility of TNBC cells. RNA sequencing was conducted, followed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses of differentially expressed genes, aiming to elucidate the potential anticancer mechanisms underlying curcumin's effects. To thoroughly elucidate the interactions among multiple proteins, we constructed a protein-protein interaction (PPI) network. Finally, the expression levels of several key proteins, including fibronectin, mTOR, β-Catenin, p-Akt, Akt, N-Cadherin, p-S6, and S6, were assessed using the western blot. The CCK8 assay results showed that curcumin significantly inhibited the proliferation of Hs578T and MDA-MB-231 cells. Flow cytometry results showed that curcumin induced apoptosis in these cells and arrested the cell cycle at the G2/M phase. Additionally, Transwell assay results showed that curcumin effectively reduced the motility of Hs578T and MDA-MB-231 cells. Enrichment analysis of RNA sequencing data showed that the mechanism of action of curcumin was significantly associated with signaling pathways such as pathways in cancer, focal adhesion, and PI3K-Akt signaling pathways. Subsequently, we constructed a protein-protein interaction network to elucidate the interactions among multiple proteins. Finally, Western blotting analysis showed that curcumin significantly decreased the expression levels of key proteins including Fibronectin, mTOR, β-Catenin, p-Akt, Akt, N-Cadherin, p-S6, and S6. Curcumin exhibits its therapeutic potential in TNBC by modulating multiple signaling pathways. It may inhibit the epithelial-mesenchymal transition process by downregulating the expression of proteins involved in the mTOR and PI3K-Akt signaling pathways, thereby suppressing the motility of TNBC cells. These findings provide experimental evidence for considering curcumin as a potential therapeutic strategy in the treatment of TNBC.
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Study on the correlation between iris blood flow, iris thickness and pupil diameter in the resting state and after pharmacological mydriasis in patients with diabetes mellitus.
Cui, L, Xiao, Y, Xiang, Z, Chen, Z, Yang, C, Zou, H
BMC ophthalmology. 2024;(1):52
Abstract
BACKGROUND To investigate whether iris blood flow and iris thickness at the iris smooth muscle region affect the pupil diameter at rest and after drug-induced mydriasis in patients with type 1 diabetes mellitus (T1DM) and type 2 diabetes mellitus (T2DM). METHODS T1DM patients and healthy children were recruited from the SCADE cohort. T2DM patients and healthy adults were recruited from patients undergoing cataract surgery at Shanghai General Hospital. Iris vessel density, pupil diameter (PD) and iris thickness were measured in both the resting and drug-induced mydriasis states. Iris vessel density was measured by optical coherence tomography angiography (OCTA), PD was measured by a pupilometer, and iris thickness at the iris smooth muscle regions were measured using anterior segment optical coherence tomography (AS-OCT). RESULTS The study included 34 pediatric T1DM patients and 50 adult T2DM patients, both groups without diabetic retinopathy, and age-sex-matched healthy controls. At baseline, T1DM children and healthy children showed no differences in iris blood flow, iris thickness, or PD. However, the adult T2DM group exhibited higher vessel density at the pupil margin, thinner iris thickness at the iris dilator region, and smaller PD compared to healthy adults, with these differences being statistically significant (P < 0.05). After pupil dilation, there were no changes in iris blood flow and PD in the T1DM group compared to healthy children, whereas the T2DM group showed a significantly smaller PD compared to healthy adults. Multivariate regression analysis revealed that in the T2DM group, glycated hemoglobin was an independent factor of PD after dilation (β=-0.490, p = 0.031), with no such factors identified in the T1DM group. CONCLUSION The insufficiently dilated pupil diameter after drug-induced mydriasis is correlated to the level of glycated hemoglobin among T2DM patients. TRIAL REGISTRATION The registration number on the clinical trial website was NCT03631108.
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Revealing the clinical effect and biological mechanism of acupuncture in COPD: A review.
Shi, F, Cao, J, Zhou, D, Wang, X, Yang, H, Liu, T, Chen, Z, Zeng, J, Du, S, Yang, L, et al
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie. 2024;:115926
Abstract
BACKGROUND To provide new ideas for the clinical and mechanism research of acupuncture in the treatment of chronic obstructive pulmonary disease (COPD), this study systematically reviews clinical research and the progress of basic research of acupuncture in the treatment of COPD. METHODS PubMed and Web of Science databases were searched using acupuncture and COPD as keywords in the last 10 years, and the included literature was determined according to exclusion criteria. FINDINGS Acupuncture can relieve clinical symptoms, improve exercise tolerance, anxiety, and nutritional status, as well as hemorheological changes (blood viscosity), reduce the inflammatory response, and reduce the duration and frequency of COPD in patients with COPD. Mechanistically, acupuncture inhibits M1 macrophage activity, reduces neutrophil infiltration, reduces inflammatory factor production in alveolar type II epithelial cells, inhibits mucus hypersecretion of airway epithelial cells, inhibits the development of chronic inflammation in COPD, and slows tissue structure destruction. Acupuncture may control pulmonary COPD inflammation through the vagal-cholinergic anti-inflammatory, vagal-adrenomedullary-dopamine, vagal-dual-sensory nerve fiber-pulmonary, and CNS-hypothalamus-orexin pathways. Furthermore, acupuncture can increase endogenous cortisol levels by inhibiting the HPA axis, thus improving airway antioxidant capacity and reducing airway inflammation in COPD. In conclusion, the inhibition of the chronic inflammatory response is the key mechanism of acupuncture treatment for COPD.
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A novel variant of DNM1L expanding the clinical phenotypic spectrum: a case report and literature review.
Zhang, Z, Bie, X, Chen, Z, Liu, J, Xie, Z, Li, X, Xiao, M, Zhang, Q, Zhang, Y, Yang, Y, et al
BMC pediatrics. 2024;(1):104
Abstract
BACKGROUND Mitochondrial diseases are heterogeneous in terms of clinical manifestations and genetic characteristics. The dynamin 1-like gene (DNM1L) encodes dynamin-related protein 1 (DRP1), a member of the GTPases dynamin superfamily responsible for mitochondrial and peroxisomal fission. DNM1L variants can lead to mitochondrial fission dysfunction. CASE PRESENTATION Herein, we report a distinctive clinical phenotype associated with a novel variant of DNM1L and review the relevant literature. A 5-year-old girl presented with paroxysmal hemiplegia, astigmatism, and strabismus. Levocarnitine and coenzyme Q10 supplement showed good efficacy. Based on the patient's clinical data, trio whole-exome sequencing (trio-WES) and mtDNA sequencing were performed to identify the potential causative genes, and Sanger sequencing was used to validate the specific variation in the proband and her family members. The results showed a novel de novo heterozygous nonsense variant in exon 20 of the DNM1L gene, c.2161C>T, p.Gln721Ter, which is predicted to be a pathogenic variant according to the ACMG guidelines. The proband has a previously undescribed clinical manifestation, namely hemiparesis, which may be an additional feature of the growing phenotypic spectrum of DNM1L-related diseases. CONCLUSION Our findings elucidate a novel variant in DNM1L-related disease and reveal an expanding phenotypic spectrum associated with DNM1L variants. This report highlights the necessity of next generation sequencing for early diagnosis of patients, and that further clinical phenotypic and genotypic analysis may help to improve the understanding of DNM1L-related diseases.
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Fertilization- and Irrigation-Modified Bacterial Community Composition and Stimulated Enzyme Activity of Eucalyptus Plantations Soil.
Huo, C, Mao, J, Zhang, J, Yang, X, Gao, S, Li, J, He, Q, Tang, G, Xie, X, Chen, Z
International journal of molecular sciences. 2024;(3)
Abstract
Irrigation and fertilization are essential management practices for increasing forest productivity. They also impact the soil ecosystem and the microbial population. In order to examine the soil bacterial community composition and structure in response to irrigation and fertilization in a Eucalyptus plantations, a total of 20 soil samples collected from Eucalyptus plantations were analyzed using high-throughput sequencing. Experimental treatments consisting of control (CK, no irrigation or fertilization), fertilization only (F), irrigation only (W), and irrigation and fertilization (WF). The results showed a positive correlation between soil enzyme activities (urease, cellulase, and chitinase) and fertilization treatments. These enzyme activities were also significantly correlated with the diversity of soil bacterial communities in Eucalyptus plantations.. Bacteria diversity was considerably increased under irrigation and fertilization (W, F, and WF) treatments when compared with the CK treatment. Additionally, the soil bacterial richness was increased in the Eucalyptus plantations soil under irrigation (W and WF) treatments. The Acidobacteria (38.92-47.9%), Proteobacteria (20.50-28.30%), and Chloroflexi (13.88-15.55%) were the predominant phyla found in the Eucalyptus plantations soil. Specifically, compared to the CK treatment, the relative abundance of Proteobacteria was considerably higher under the W, F, and WF treatments, while the relative abundance of Acidobacteria was considerably lower. The contents of total phosphorus, accessible potassium, and organic carbon in the soil were all positively associated with fertilization and irrigation treatments. Under the WF treatment, the abundance of bacteria associated with nitrogen and carbon metabolisms, enzyme activity, and soil nutrient contents showed an increase, indicating the positive impact of irrigation and fertilization on Eucalyptus plantations production. Collectively, these findings provide the scientific and managerial bases for improving the productivity of Eucalyptus plantations.
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Gut microbiota and its metabolites in Alzheimer's disease: from pathogenesis to treatment.
Zou, X, Zou, G, Zou, X, Wang, K, Chen, Z
PeerJ. 2024;:e17061
Abstract
INTRODUCTION An increasing number of studies have demonstrated that altered microbial diversity and function (such as metabolites), or ecological disorders, regulate bowel-brain axis involvement in the pathophysiologic processes in Alzheimer's disease (AD). The dysregulation of microbes and their metabolites can be a double-edged sword in AD, presenting the possibility of microbiome-based treatment options. This review describes the link between ecological imbalances and AD, the interactions between AD treatment modalities and the microbiota, and the potential of interventions such as prebiotics, probiotics, synbiotics, fecal microbiota transplantation, and dietary interventions as complementary therapeutic strategies targeting AD pathogenesis and progression. SURVEY METHODOLOGY Articles from PubMed and china.com on intestinal flora and AD were summarized to analyze the data and conclusions carefully to ensure the comprehensiveness, completeness, and accuracy of this review. CONCLUSIONS Regulating the gut flora ecological balance upregulates neurotrophic factor expression, regulates the microbiota-gut-brain (MGB) axis, and suppresses the inflammatory responses. Based on emerging research, this review explored novel directions for future AD research and clinical interventions, injecting new vitality into microbiota research development.
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Mechanisms and therapeutic targets of mitophagy after intracerebral hemorrhage.
Huang, Q, Yu, X, Fu, P, Wu, M, Yin, X, Chen, Z, Zhang, M
Heliyon. 2024;(1):e23941
Abstract
Mitochondria are dynamic organelles responsible for cellular energy production. In addition to regulating energy homeostasis, mitochondria are responsible for calcium homeostasis, clearance of damaged organelles, signaling, and cell survival in the context of injury and pathology. In stroke, the mechanisms underlying brain injury secondary to intracerebral hemorrhage are complex and involve cellular hypoxia, oxidative stress, inflammatory responses, and apoptosis. Recent studies have shown that mitochondrial damage and autophagy are essential for neuronal metabolism and functional recovery after intracerebral hemorrhage, and are closely related to inflammatory responses, oxidative stress, apoptosis, and other pathological processes. Because hypoxia and inflammatory responses can cause secondary damage after intracerebral hemorrhage, the restoration of mitochondrial function and timely clearance of damaged mitochondria have neuroprotective effects. Based on studies on mitochondrial autophagy (mitophagy), cellular inflammation, apoptosis, ferroptosis, the BNIP3 autophagy gene, pharmacological and other regulatory approaches, and normobaric oxygen (NBO) therapy, this article further explores the neuroprotective role of mitophagy after intracerebral hemorrhage.