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1.
J Neurointerv Surg ; 2024 Feb 22.
Article in English | MEDLINE | ID: mdl-38388478

ABSTRACT

A brain-computer interface (BCI) serves as a direct communication channel between brain activity and external devices, typically a computer or robotic limb. Advances in technology have led to the increasing use of intracranial electrical recording or stimulation in the treatment of conditions such as epilepsy, depression, and movement disorders. This indicates that BCIs can offer clinical neurological rehabilitation for patients with disabilities and functional impairments. They also provide a means to restore consciousness and functionality for patients with sequelae from major brain diseases. Whether invasive or non-invasive, the collected cortical or deep signals can be decoded and translated for communication. This review aims to provide an overview of the advantages of endovascular BCIs compared with conventional BCIs, along with insights into the specific anatomical regions under study. Given the rapid progress, we also provide updates on ongoing clinical trials and the prospects for current research involving endovascular electrodes.

2.
Materials (Basel) ; 15(5)2022 Mar 07.
Article in English | MEDLINE | ID: mdl-35269196

ABSTRACT

Electric furnace ferronickel slag (EFS) is a typical magnesium-rich industrial by-product discharged from the manufacture of nickel and iron-nickel alloys. The approach to use it as the raw material for the preparation of magnesium phosphate cement (MPC) has potential and proves effective. In this study, three different phosphorus sources (PS) including phosphoric acid (H3PO4, PA), sodium dihydrogen phosphate (NaH2PO4, SDP) and potassium dihydrogen phosphate (KH2PO4, PDP) were used to react with EFS to prepare the EFS-based MPC (EMPC), and the effects of raw material mass ratio (EFS/PA, EFS/SDP, EFS/PDP) on the compressive strength, early hydration temperature and microstructure of EMPC pastes were investigated. Results showed that the compressive strength of EMPC paste is significantly impacted by the type of phosphorus source and the raw materials mass ratio. When the EFS/PDP ratio is 4.0, the compressive strength of the MPC paste reaches up to 18.8, 22.8 and 27.5 MPa at 3, 7 and 28 d, respectively. Cattiite (Mg3(PO4)2·22H2O), K-struvite (KMgPO4·6H2O) and/or Na-struvite (NaMgPO4·6H2O) were identified as the main hydration products of EMPC. The development of EMPC mainly involves the dissolution of a phosphorus source, MgO and Mg2SiO4, formation of hydration product as binder, and combination of the unreacted raw materials together by binders to build a compact form.

3.
Environ Technol ; 43(19): 2881-2890, 2022 Aug.
Article in English | MEDLINE | ID: mdl-33755530

ABSTRACT

Removal and immobilization of highly toxic arsenic form industrial wastewater using simple and effective methods is of important practical significance. Although the formation of natroalunite phase NaAl3(SO4)2(OH)6 has been demonstrated to be an effective method for arsenic immobilization in model system with chemical reagent grade arsenates as arsenic source, the further study is needed to investigate its immobilization for real industrial wastewater. This work reported the synthesis of natroalunite phase NaAl3(SO4)2(OH)6 using arsenic-containing industrial wastewater from benzyl acid production. The synthesis temperature and time were optimized to obtain the pure natroalunite phase composites with high crystallinity. When n(Al/As)aq was greater than 3.0, the arsenic could almost precipitate exclusively as natroalunite phase after 60 min hydrothermal reaction at 200°C, with a maximum arsenic immobilization amount of 7.0 mol%. A maximum leaching concentration of 0.50 mg/L was observed at pH = 3.0 during the short-term (24 h) leaching test, which was lower than the US EPA TCLP test limit of 1 mg/L. The long-term leaching test up to 90 days revealed that the arsenonatroalunite could be a safe immobilization material for arsenic in pH 5.0-8.0 environments.


Subject(s)
Arsenic , Arsenates , Arsenic/analysis , Hydrogen-Ion Concentration , Wastewater
5.
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-793244

ABSTRACT

@#非编码RNA(ncRNA)是一类不具有编码蛋白功能的RNA转录本,其异常表达参与了肿瘤的发生与发展。ncRNA的 组织特异性表达使其具有鉴别肿瘤,甚至具有对肿瘤分型、分期的应用潜能。雌激素受体阴性(ER-)乳腺癌是指不表达ER的乳 腺癌,其治疗困难、预后极差、病死率居乳腺癌之首。ncRNA在ER-乳腺癌中存在差异表达,并可通过参与非雌激素激活通路在乳 腺癌的发生发展及预后过程中起重要调控作用。本文拟针对ncRNA中的微小RNA(miRNA)、长链非编码RNA(lncRNA)、环状 RNA(circRNA)在ER-乳腺癌中的作用展开综述,分析它们在临床中的应用价值, 为ER-乳腺癌的早期诊断及预后判断提供新的 分子标志物和监测手段。

6.
Acta Biochim Biophys Sin (Shanghai) ; 50(8): 776-781, 2018 Aug 01.
Article in English | MEDLINE | ID: mdl-29939221

ABSTRACT

Multiple independent reports have demonstrated pericyte loss in both the hippocampus and cortex in human Alzheimer's disease (AD). The differentiation and recruitment of pericytes are the essential steps in vasculature development. However, the role of amyloid beta (Aß) in pericyte differentiation has not yet been fully elucidated. In this study, we investigated the interaction between Aß and differentiation of mesenchymal stem cells (MSCs) toward pericytes in culture. Our results showed that mice overexpressing Aß-precursor protein (APP/PS1) exhibited the loss of pericytes compared with the control group mice, evidenced by the lack of desmin expression in the cortex of 12-month-old mice. Interestingly, we further found that both Aß40 and Aß42 inhibited the expressions of pericyte markers (α-SMA, desmin, and PDGFRß) in cultured MSCs which can be differentiated into mature pericytes. Mechanistically, the inhibitory effects of Aßs on MSC-pericyte transition is mediated by the activation of the ERK1/2 MAPK signal pathway. These new insights into the roles of Aß in pericyte differentiation may help to develop more effective strategies for the treatment of AD.


Subject(s)
Amyloid beta-Peptides/pharmacology , Cell Differentiation/drug effects , MAP Kinase Signaling System/drug effects , Mesenchymal Stem Cells/drug effects , Pericytes/drug effects , Alzheimer Disease/genetics , Alzheimer Disease/metabolism , Amyloid beta-Protein Precursor/genetics , Amyloid beta-Protein Precursor/metabolism , Animals , Cells, Cultured , Desmin/genetics , Desmin/metabolism , Gene Expression , Humans , Mesenchymal Stem Cells/cytology , Mesenchymal Stem Cells/metabolism , Mice, Inbred C57BL , Mice, Transgenic , Pericytes/cytology , Pericytes/metabolism , Presenilin-1/genetics , Presenilin-1/metabolism
7.
J Environ Manage ; 191: 58-65, 2017 Apr 15.
Article in English | MEDLINE | ID: mdl-28086141

ABSTRACT

Low-carbon ferrochrome slag (LCFS), a by-product of the ferrochrome alloy industry, has potential for use as a cementitious material due to its pozzolanic characteristic. The objective of the present study was to determine the optimum compound chemical activators for LCFS-based composite cement using an orthogonal test, in which 7 d and 28 d compressive strengths were used as the evaluating indices. The influences of compound chemical activators on the hydration of a composite cement mix were investigated using X-ray diffraction (XRD), scanning electron microscopy with energy dispersive X-ray spectroscopy (SEM/EDS) and thermogravimetry-differential scanning calorimetry (TG-DSC). The optimum activator to activate the composite cement was a compound of NaCl (NC) at a dosage of 0.6%, Na2SO4 (NS) at a dosage of 1.2%, NaF (NF) at a dosage of 0.6% and Al2(SO4)3 (AS) at a dosage of 0.9% or 0.7%. The compressive strengths of the optimum composite cement mix at ages of 3, 28 and 180 d increased by 50.1%, 22.4% and 16.5%, respectively. More hydration products including ettringite and calcium silicate hydrate were formed at an early age of hydration. The compound chemical activators effectively activated the ferrochrome slag (FS), blast-furnace slag (BFS) and fly ash (FA) in the composite cement.


Subject(s)
Carbon/chemistry , Construction Materials , Coal Ash/chemistry , Spectrometry, X-Ray Emission , X-Ray Diffraction
8.
J Neuroimmune Pharmacol ; 7(3): 640-55, 2012 Sep.
Article in English | MEDLINE | ID: mdl-22684353

ABSTRACT

Despite FDA suspension of Elan's AN-1792 amyloid beta (Aß) vaccine in phase IIb clinical trials, the implications of this study are the guiding principles for contemporary anti-Aß immunotherapy against Alzheimer's disease (AD). AN-1792 showed promising results with regards to Aß clearance and cognitive function improvement, but also exhibited an increased risk of Th1 mediated meningoencephalitis. As such, vaccine development has continued with an emphasis on eliciting a notable anti-Aß antibody titer, while avoiding the unwanted Th1 pro-inflammatory response. Previously, we published the first report of an Aß sensitized dendritic cell vaccine as a therapeutic treatment for AD in BALB/c mice. Our vaccine elicited an anti-Aß titer, with indications that a Th1 response was not present. This study is the first to investigate the efficacy and safety of our dendritic cell vaccine for the prevention of AD in transgenic mouse models (PDAPP) for AD. We also used Immunohistochemistry to characterize the involvement of LXR, ABCA1, and CD45 in order to gain insight into the potential mechanisms through which this vaccine may provide benefit. The results indicate that (1) the use of mutant Aß1-42 sensitized dendritic cell vaccine results in durable antibody production, (2) the vaccine provides significant benefits with regards to cognitive function without the global (Th1) inflammation seen in prior Aß vaccines, (3) histological studies showed an overall decrease in Aß burden, with an increase in LXR, ABCA1, and CD45, and (4) the beneficial results of our DC vaccine may be due to the LXR/ABCA1 pathway. In the future, mutant Aß sensitized dendritic cell vaccines could be an efficacious and safe method for the prevention or treatment of AD that circumvents problems associated with traditional anti-Aß vaccines.


Subject(s)
Alzheimer Disease/pathology , Alzheimer Disease/prevention & control , Alzheimer Vaccines/therapeutic use , Amyloid beta-Peptides/genetics , Dendritic Cells/transplantation , Mutation/genetics , Peptide Fragments/genetics , Vaccines, DNA/administration & dosage , Alzheimer Disease/genetics , Alzheimer Vaccines/administration & dosage , Alzheimer Vaccines/genetics , Amino Acid Sequence , Amyloid beta-Peptides/administration & dosage , Amyloid beta-Peptides/therapeutic use , Animals , Female , Male , Mice , Mice, Inbred C57BL , Mice, Transgenic , Molecular Sequence Data , Peptide Fragments/administration & dosage , Peptide Fragments/therapeutic use , Treatment Outcome , Vaccines, DNA/genetics , Vaccines, DNA/therapeutic use
9.
Zhongguo Zhong Yao Za Zhi ; 34(8): 1027-31, 2009 Apr.
Article in Chinese | MEDLINE | ID: mdl-19639794

ABSTRACT

OBJECTIVE: To investigate the suppressive effect of resveratrol on growth of U251 human glioma cells and its correlated mechanism. METHOD: U251 human glioma cells were treated with resveratrol at various concentrations, MTT assay was used to determine the inhibitory rate of cell proliferation, FCM to detect the cell apoptosis, the expressions of Bcl-2, Bcl-XL, STAT3 and CyclinD1 were analysed by immunohistochemistry and Western blot to examine the expression of Bcl-2, Bcl-XL, STAT3, CyclinD1, Caspase-3 and Bax. RESULT: After treatment with resveratrol, MTT assay showed the growth of U251 cells was inhibited in dose-dependent and time-dependent manners, apoptosis of cells advanced stage was built up, immunohistochemical staining displayed decreased the expression of Bcl-2, Bcl-XL, STAT3 and CyclinD1 and Western blot showed that resveratrol decreased the expression of Bcl-2, Bcl-XL, STAT3 and CyclinD1, and built up Bax and Caspase-3. CONCLUSION: It is possible that downregulated the expression of Bcl-2, Bcl-XL, but upregulated Bax and Caspase-3, and the indication was obviously in dose-dependent and time-dependent manners.


Subject(s)
Glioma/drug therapy , Glioma/metabolism , Stilbenes/therapeutic use , Apoptosis/drug effects , Blotting, Western , Caspase 3/metabolism , Cell Line, Tumor , Cyclin D1/metabolism , Gene Expression Regulation, Neoplastic/drug effects , Humans , Immunohistochemistry , Proto-Oncogene Proteins c-bcl-2/metabolism , Resveratrol , STAT3 Transcription Factor/metabolism , bcl-2-Associated X Protein/metabolism , bcl-X Protein/metabolism
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