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1.
J Cell Physiol ; 236(2): 1116-1130, 2021 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-32730644

RESUMO

Breast cancer is one of the most threatening diseases for women. Long noncoding RNAs were reported to be involved in breast cancer development. In this study, we analyzed The Cancer Genome Atlas breast cancer tissue high-throughput sequencing data and screened and validated the low-expressing long noncoding RNA named MAGI2-AS3. Through gene coexpression analysis, we found that MAGI2-AS3 has a good expression correlation with MAGI2. Overexpression of MAGI2-AS3 or MAGI2 in breast cancer cells MCF-7 would inhibit the Wnt/ß-catenin pathway and inhibit cell proliferation and migration. Gene structure and DNA methylation analysis results indicated that MAGI2-AS3 may act as a cis-acting regulatory element downregulating the DNA methylation level of the MAGI2 promoter region, and the DNA demethylase TET1 inhibitor can reverse MAGI2-AS3 overexpression caused upregulation of MAGI2 and cellular effects. Our findings reveal the role of MAGI2-AS3 in breast cancer and provide potential novel therapeutic targets for metastatic breast cancer intervention.

2.
Int J Biol Sci ; 16(15): 2951-2963, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33061808

RESUMO

Previous studies have demonstrated that the antitumor potential of IU1 (a pharmacological compound), which was mediated by selective inhibition of proteasome-associated deubiquitinase ubiquitin-specific protease 14 (USP14). However, the underlying molecular mechanisms remain elusive. It has been well established that mdm2 (Murine double minute 2) gene was amplified and/or overexpressed in a variety of human neoplasms, including cervical cancer. Furthermore, MDM2 is critical to cervical cancer development and progression. Relatively studies have reported that USP15 and USP7 stabilized MDM2 protein levels by removing its ubiquitin chain. In the current study, we studied the cell proliferation status after IU1 treatment and the USP14-MDM2 protein interaction in cervical cancer cells. This study experimentally revealed that IU1 treatment reduced MDM2 protein expression in HeLa cervical cancer cells, along with the activation of autophagy-lysosomal protein degradation and promotion of ubiquitin-proteasome system (UPS) function, thereby blocked G0/G1 to S phase transition, decreased cell growth and triggered cell apoptosis. Thus, these results indicate that IU1 treatment simultaneously targets two major intracellular protein degradation systems, ubiquitin-proteasome and autophagy-lysosome systems, which leads to MDM2 degradation and contributes to the antitumor effect of IU1.

3.
Front Med (Lausanne) ; 7: 436, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32850917

RESUMO

Background: The kidney is a target organ that could be infected by SARS-CoV-2, and acute kidney injury (AKI) was associated with a higher risk of COVID-19 patients' in-hospital death. However, no published works discussed about the risk factors of COVID-19 related AKI. Methods: We conducted a retrospective cohort study, recruiting COVID-19 inpatients from the Sino-French branch of Tongji Hospital. Demographic, clinical, treatment, and laboratory data were collected and compared. We used univariable and multivariable logistic regression methods to identify the risk factors of COVID-19-related AKI. Results: Of the 116 patients in our study, 12 (10.3%) were recognized as AKI, including 5 (4.3%) in-hospital AKI. Multivariable regression showed increasing odds of COVID-19-related AKI associated with COVID-19 clinical classification (OR = 8.155, 95% CI = 1.848-35.983, ref = non-critical, p = 0.06), procalcitonin more than 0.1 ng/mL (OR = 4.822, 95% CI = 1.095-21.228, p = 0.037), and estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m2 (OR = 13.451, 95% CI = 1.617-111.891, p = 0.016). Conclusions: COVID-19-related AKI was likely to be related to multiorgan failure rather than the kidney tropism of SARS-CoV-2. The potential risk factors of COVID-19 clinical classification, procalcitonin more than 0.1 ng/mL, and eGFR <60 mL/min/1.73 m2 could help clinicians to identify patients with kidney injury at an early stage.

4.
Eur J Pharmacol ; 889: 173493, 2020 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-32860808

RESUMO

Gastric cancer (GC) is one of the most common malignant neoplasms of the digestive system, with China leading in terms of morbidity and mortality rates. Betulinic acid (BA) is a widely-occurring pentacyclic triterpenoid that has been reported to exhibit potent anti-inflammatory, antioxidant, and antitumor activities. BA can combat tumors by inducing apoptosis, regulating cell cycle, and inhibiting autophagy, but its mechanism of action in the context of GC is unclear. A preliminary study found that higher expression of vasodilator-stimulated phosphoprotein (VASP) was correlated with migration in the GC cell line. In this study, BGC-823 cells and MNK45 cells were treated with BA for investigating its effect on the proliferation and migration of cells. Moreover, the expression of VASP and upstream signal molecules were also investigated in this background. The results showed BA could inhibit the proliferation and migration the GC cells. Furthermore, NF-κB acted as a transcription factor to upregulate VASP expression. Moreover, BA could downregulate the expression of VASP at the protein and mRNA level by inhibiting NF-κB activity. In conclusion, these results suggest that BA could inhibit the expression of VASP by negatively regulating NF-κB, thereby inhibiting the proliferation and migration of the GC cells. Our study provides a theoretical basis for exploring the molecular mechanism underlying BA-induced inhibition of proliferation and migration in GC cells.

5.
Mol Cancer ; 19(1): 128, 2020 08 24.
Artigo em Inglês | MEDLINE | ID: mdl-32838810

RESUMO

BACKGROUND: Deregulated circular RNAs (circRNAs) are associated with the development of cancer and therapy resistance. However, functional research of circRNAs mostly focus on potential miRNA or protein binding and more potential regulation of circRNA on host gene DNA in cancers are yet to be inspected. METHOD: We performed total RNA sequencing on clinical breast cancer samples and identified the expression patterns of circRNAs and corresponding host genes in patient blood, tumor and adjacent normal tissues. qPCR, northern blot and in situ hybridization were used to validate the dysregulation of circRNA circSMARCA5. A series of procedures including R-loop dot-blotting, DNA-RNA immunoprecipitation and mass spectrum, etc. were conducted to explore the regulation of circSMARCA5 on the transcription of exon 15 of SMARCA5. Moreover, immunofluorescence and in vivo experiments were executed to investigate the overexpression of circSMARCA5 with drug sensitivities. RESULTS: We found that circRNAs has average higher expression over its host linear genes in peripheral blood. Compared to adjacent normal tissues, circSMARCA5 is decreased in breast cancer tissues, contrary to host gene SMARCA5. The enforced expression of circSMARCA5 induced drug sensitivity of breast cancer cell lines in vitro and in vivo. Furthermore, we demonstrated that circSMARCA5 can bind to its parent gene locus, forming an R-loop, which results in transcriptional pausing at exon 15 of SMARCA5. CircSMARCA5 expression resulted in the downregulation of SMARCA5 and the production of a truncated nonfunctional protein, and the overexpression of circSMARCA5 was sufficient to improve sensitivity to cytotoxic drugs. CONCLUSION: Our results revealed a new regulatory mechanism for circRNA on its host gene and provided evidence that circSMARCA5 may serve as a therapeutic target for drug-resistant breast cancer patients.

6.
Folia Histochem Cytobiol ; 57(2): 56-63, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31112282

RESUMO

INTRODUCTION: Long interspersed nuclear elements-1 (L1), as the only one self-active retrotransposon of the mobile element, was found to be generally activated in tumor cells. The 5'UTR of L1 (L1-5'UTR) contains both sense and antisense bidirectional promoters, transcription products of which can generate double-strand RNA (dsRNA). In addition, L1-ORF1p, a dsRNA binding protein encoded by L1, is considered to engage in some RNA-protein (RNP) formation. Ago2, one of the RISC components, can bind to dsRNA to form RISC complex, but its role in L1 regulation still remains unclear. Due that the 5'UTR of L1 (L1-5'UTR) contains both sense and antisense bidirectional promoters, so the activities in both string were identified. A dsRNA-mediated regulation of L1-5'UTR, with the feedback regulation of L1-ORF1p as well as other key molecules engaged (Ago1-4) in this process, was also investigated. MATERIAL AND METHODS: Genomic DNA was extracted from HEK293 cells and subjected to L1-5'UTR prepa-ration by PCR. Report gene system pIRESneo with SV40 promoter was employed. The promoter activities of different regions in L1-5'UTR were identified by constructing these regions into pIRESneo, which SV40 region was removed prior, to generate different recombinant plasmids. The promoter activities in recombinant plasmids were detected by the luciferase expression assay. Western blot and co-immunoprecipitation were employed to identify proteins expression and protein-protein interaction respectively. RESULTS: Ago2 is a member of Agos family, which usually forms a RISC complex with si/miRNA and is involved in post- transcriptional regulation of many genes. Here L1-ORF1p and Ago2 conducts a regulation as a negative feedback for L1-5'UTR sense promoter. L1-ORF1p could form the immune complexes with Ago1, Ago2 and Ago4, respectively. CONCLUSIONS: L1-5'UTR harbors both sense and antisense promoter activity and a dsRNA-mediated regulation is responsible for L1-5'UTR regulation. Agos proteins and L1-ORF1p were engaged in this process.


Assuntos
Regiões 5' não Traduzidas , Proteínas Argonauta/genética , Regulação da Expressão Gênica , Elementos Nucleotídeos Longos e Dispersos , RNA Interferente Pequeno/genética , Ribonucleoproteínas/genética , Sequência de Bases , Células HEK293 , Humanos , Mutação , Regiões Promotoras Genéticas
7.
Biomed Res Int ; 2019: 3235021, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31011573

RESUMO

Background: Breast cancer (BC) is one of the most common malignant tumors in women around the world. Atorvastatin (ATO) was found to be associated with a decreased risk of recurrence and mortality in cancer. But the exact mechanism of its carcinostatic effects is unclear. The expression level of Ras homolog family member B (RhoB) in breast cancer cells was found to be upregulated after being treated with ATO. Thus, we conjecture that altered expression of RhoB induced by ATO may be decisive for the migration and progression of breast cancer. Methods: The effects of ATO on breast tumor cells in vivo and in vitro were detected by clone formation assay, CCK-8 assay, flow cytometry, wound healing, transwell assays, tumor xenograft model, and immunohistochemistry. Distribution of RhoB in different breast cancer tissues and its influence on prognosis were analyzed using the data from TCGA or GEO databases. The relationship between RhoB and PTEN/AKT pathway was detected by Western blotting and RT-qPCR. Results: ATO inhibits proliferation, invasion, EMT, and PTEN/AKT pathway and promotes apoptosis in breast tumor cells. In addition, ATO inhibits the volume and weight of breast tumor in tumor-bearing mice and upregulated RhoB in tumor tissues. The expression of RhoB in mRNA and protein level was upregulated in statin-treated breast cancer cells and downregulated in cancer tissues. Low expression of RhoB links with poor prognosis in patients with breast cancer (HR = 0.74[0.66-0.83], p =7e-8, log-rank test). Further research found that RhoB inhibits the proliferation, invasion, EMT, and PTEN/AKT signal pathway in breast tumor cells. Conclusions: The exact mechanism of ATO's carcinostatic effects in breast cancer is related to downregulating PTEN/AKT pathway via promoting RhoB. Our study also demonstrates the potential applicability of RhoB as a therapeutic target for breast cancer.


Assuntos
Atorvastatina/farmacologia , Neoplasias da Mama/tratamento farmacológico , Regulação para Baixo/efeitos dos fármacos , PTEN Fosfo-Hidrolase/genética , Proteínas Proto-Oncogênicas c-akt/genética , Transdução de Sinais/efeitos dos fármacos , Proteína rhoB de Ligação ao GTP/genética , Animais , Apoptose/efeitos dos fármacos , Apoptose/genética , Neoplasias da Mama/genética , Linhagem Celular Tumoral , Movimento Celular/efeitos dos fármacos , Movimento Celular/genética , Proliferação de Células/efeitos dos fármacos , Proliferação de Células/genética , Regulação para Baixo/genética , Feminino , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Regulação Neoplásica da Expressão Gênica/genética , Humanos , Células MCF-7 , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Nus , Recidiva Local de Neoplasia/genética , Prognóstico , Transdução de Sinais/genética , Regulação para Cima/efeitos dos fármacos , Regulação para Cima/genética , Ensaios Antitumorais Modelo de Xenoenxerto/métodos
8.
Phys Chem Chem Phys ; 19(35): 23960-23970, 2017 Sep 13.
Artigo em Inglês | MEDLINE | ID: mdl-28831469

RESUMO

HCN being a highly toxic N-containing volatile organic compound (VOCs) poses great threat to human living environment. Selective catalytic combustion of HCN (HCN-SCC) over metal modified zeolite catalysts has attracted great attention due to related high efficiency and excellent N2 selectivity. In the present work, three types of 24T-Cu-BEA models with different active centers of single [Cu]+, double [Cu]+, and [Cu-O-Cu]2+ were constructed for HCN-SCC mechanism simulations based on density functional theory (DFT). DFT simulation results revealed that HCN-SCC followed an oxidation mechanism over double [Cu]+ through an intermediate of NCO, wherein the synergistic effects of double [Cu]+ active centers were clearly observed, resulting in a significantly lowered energy barrier (1.6 kcal mol-1) during HCN oxidation into NCO. However, an oxidation mechanism (HCN oxidized into NH radical and CO2 through intermediate of HNCO) combining with a hydrolysis mechanism (NH radical hydrolyses into NH3) occurred over single [Cu]+ and [Cu-O-Cu]2+, wherein the NH2 hydrolysis to NH3 step was regarded as the rate determining step with an energy barrier of 72.3 and 74.3 kcal mol-1, respectively. Finally, Mulliken charge transfer (CT) analysis was conducted, based on which the electric properties of different active centers were well illustrated.

9.
Oncol Rep ; 38(3): 1733-1741, 2017 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-28677734

RESUMO

SE translocation (SET) oncoprotein, an inhibitor of protein phosphatase 2A, is abnormally expressed in many cancers. In this study, SET was aberrantly upregulated in gastric cancer (GC) compared with control tissues. Clinicopathological analysis showed that SET expression was significantly correlated with pathological grade (p=0.002), lymph node stage (p=0.014), and invasive depth (p=0.022). Kaplan-Meier analysis indicated that patients with high SET expression showed poorer overall survival rates than those with low SET expression. Moreover, SET knockdown downregulated GC cell proliferation, colony formation, tumorigenesis, and metastasis. The biological effect of SET on proliferation and invasion was mediated by inhibition of protein phosphatase 2, which in turn, activated Akt. Taken together, our results suggested that SET overexpression is associated with GC progression, and it might be a potential diagnostic marker for GC, thereby a possible target for GC drug development.


Assuntos
Chaperonas de Histonas/genética , Proteínas Oncogênicas/genética , Neoplasias Gástricas/genética , Fatores de Transcrição/genética , Animais , Biomarcadores Tumorais/genética , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células/genética , Proteínas de Ligação a DNA , Progressão da Doença , Regulação Neoplásica da Expressão Gênica/genética , Humanos , Estimativa de Kaplan-Meier , Metástase Linfática/genética , Metástase Linfática/patologia , Masculino , Camundongos , Camundongos Nus , Pessoa de Meia-Idade , Invasividade Neoplásica/genética , Invasividade Neoplásica/patologia , Prognóstico , Proteína Fosfatase 2/genética , Neoplasias Gástricas/patologia , Taxa de Sobrevida , Translocação Genética/genética , Regulação para Cima/genética
10.
Oncol Rep ; 38(1): 598-606, 2017 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-28560452

RESUMO

We have shown that a novel STAT3 inhibitor arctigenin (Atn) induces significant cytotoxicity in triple-negative breast cancer (TNBC) cells. This study further delineated molecular mechanisms where by Atn triggered cytotoxicity in TNBC cells. We found Atn can also inhibit metastasis in TNBC cells through cancerous inhibitor of protein phosphatase 2A (CIP2A) pathway. CIP2A is an endogenous inhibitor of protein phosphatase 2A (PP2A), which can increase the migration and invasion of various cancer cells. PP2A is a tumor suppressor, which is functionally defective in various cancers. Atn-induced metastasis inhibition was associated with reactivation of PP2A, downregulation of CIP2A and Akt phosphorylation. Silencing CIP2A enhanced Atn-induced metastasis inhibition and apoptosis in TNBCs. Furthermore, ectopic expression of CIP2A or inhibition of PP2A in TNBC cells abolished the effects of Atn. In conclusion, we found that enhancement of PP2A activity by inhibition of CIP2A, at least in part, promotes the anti-metastasis effect induced by Atn. Our findings disclose the novel therapeutic mechanism of this targeted agent, and suggest the therapeutic potential and feasibility of developing PP2A enhancers as a novel anticancer strategy.


Assuntos
Antineoplásicos/farmacologia , Autoantígenos/metabolismo , Furanos/farmacologia , Lignanas/farmacologia , Proteínas de Membrana/metabolismo , Proteína Fosfatase 2/metabolismo , Neoplasias de Mama Triplo Negativas/tratamento farmacológico , Antineoplásicos/uso terapêutico , Apoptose , Autoantígenos/genética , Linhagem Celular Tumoral , Regulação para Baixo , Furanos/uso terapêutico , Humanos , Peptídeos e Proteínas de Sinalização Intracelular , Lignanas/uso terapêutico , Proteínas de Membrana/genética , Fosforilação , Proteínas Proto-Oncogênicas c-akt/metabolismo , Interferência de RNA , RNA Interferente Pequeno/metabolismo , Fator de Transcrição STAT3/metabolismo , Transdução de Sinais/efeitos dos fármacos , Neoplasias de Mama Triplo Negativas/patologia
11.
Oncol Rep ; 38(1): 271-278, 2017 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-28534965

RESUMO

Cancerous inhibitor of protein phosphatase 2A (CIP2A) is a human oncoprotein that is overexpressed in multiple kinds of tumors including gastric cancer (GC). Mammalian target of rapamycin complex 1 (mTORC1) over-activation is detected in GC and many other cancers. Previous study found that CIP2A/mTORC1 controls cell growth and autophagy through direct association. CIP2A plays an 'oncogenic nexus' in several cancer types to participate in the tumorigenic transformation and chemoresistance. In the present study, we investigated whether Cucurbitacin B (CuB), a natural compound found in Cucurbitaceae, can be used in cisplatin (DDP)-resistant human GC cell line SGC7901/DDP. Results demonstrated that CuB treatment significantly suppressed SGC7901/DDP cell proliferation, induced caspase-dependent apoptosis, and autophagy. The activation of autophagy was mediated through CuB-induced inhibition of mTORC1. Furthermore, CuB inhibited mTORC1 via the activation of protein phosphatase 2A (PP2A) which is mediated by CIP2A inhibition. These findings indicated that CuB can inhibit the proliferation, induce caspase-dependent apoptosis, and autophagy of SGC7901/DDP cells by suppressing CIP2A/PP2A/mTORC1 signaling axis. Thus, CuB may be a novel effective candidate to treat DDP-resistant human GC cells.


Assuntos
Apoptose/efeitos dos fármacos , Autofagia/efeitos dos fármacos , Cisplatino/farmacologia , Resistencia a Medicamentos Antineoplásicos/efeitos dos fármacos , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Neoplasias Gástricas/patologia , Triterpenos/farmacologia , Antineoplásicos/farmacologia , Autoantígenos/metabolismo , Proliferação de Células/efeitos dos fármacos , Humanos , Peptídeos e Proteínas de Sinalização Intracelular , Alvo Mecanístico do Complexo 1 de Rapamicina/metabolismo , Proteínas de Membrana/metabolismo , Proteína Fosfatase 2/metabolismo , Transdução de Sinais , Neoplasias Gástricas/tratamento farmacológico , Neoplasias Gástricas/metabolismo , Células Tumorais Cultivadas
12.
Biomaterials ; 132: 59-71, 2017 07.
Artigo em Inglês | MEDLINE | ID: mdl-28407495

RESUMO

Interest in non-invasive injectable therapies has rapidly risen due to their excellent safety profile and ease of use in clinical settings. Injectable hydrogels can be derived from the extracellular matrix (ECM) of specific tissues to provide a biomimetic environment for cell delivery and enable seamless regeneration of tissue defects. We investigated the in situ delivery of human mesenchymal stem cells (hMSCs) in decellularized meniscus ECM hydrogel to a meniscal defect in a nude rat model. First, decellularized meniscus ECM hydrogel retained tissue-specific proteoglycans and collagens, and significantly upregulated expression of fibrochondrogenic markers by hMSCs versus collagen hydrogel alone in vitro. The meniscus ECM hydrogel in turn supported delivery of hMSCs for integrative repair of a full-thickness defect model in meniscal explants after in vitro culture and in vivo subcutaneous implantation. When applied to an orthotopic model of meniscal injury in nude rat, hMSCs in meniscus ECM hydrogel were retained out to eight weeks post-injection, contributing to tissue regeneration and protection from joint space narrowing, pathologic mineralization, and osteoarthritis development, as evidenced by macroscopic and microscopic image analysis. Based on these findings, we propose the use of tissue-specific meniscus ECM-derived hydrogel for the delivery of therapeutic hMSCs to treat meniscal injury.


Assuntos
Hidrogel de Polietilenoglicol-Dimetacrilato/química , Menisco/patologia , Transplante de Células-Tronco Mesenquimais , Cicatrização , Animais , Adesão Celular , Técnicas de Cultura de Células , Proliferação de Células , Sistemas de Liberação de Medicamentos , Matriz Extracelular/patologia , Feminino , Membro Posterior , Humanos , Masculino , Fenômenos Mecânicos , Menisco/lesões , Camundongos Nus , Ratos Nus , Regeneração , Engenharia Tecidual
13.
Phys Chem Chem Phys ; 19(11): 7971-7979, 2017 Mar 15.
Artigo em Inglês | MEDLINE | ID: mdl-28263332

RESUMO

A series of zeolite catalysts, M(Cu, Fe, Co)-ZSM-5, was prepared by an impregnation method and evaluated for the selective catalytic combustion of acrylonitrile (AN-SCC). Cu-ZSM-5, exhibiting the highest AN conversion activity and best N2 yield, was further selected for an AN-SCC mechanism investigation, wherein both experimental [in situ diffuse reflectance infrared Fourier transform spectroscopy (DRIFTS)] and theoretical [density functional theory (DFT)] approaches were employed. The in situ DRIFTS revealed that AN-SCC followed a hydrolysis mechanism at T < 300 °C via intermediates of acylamino species (-CONH2) and NH3, while it followed an oxidation mechanism at T > 300 °C via an intermediate of NCO. The DFT simulations gave much deeper insights suggesting that: (i) the NCO could be generated by oxidation of AN over [Cu]+ active sites, with an assistance of dissociated atomic O from gaseous O2; (ii) three types of reaction routes could be proposed for the further reaction of NCO to produce N2, namely NCO direct dissociation, NCO coupling, and NO + NCO reaction; and (iii) the last route (NO + NCO), possessing the lowest energy barrier, was the most probable reaction pathway, wherein the NO could be produced by oxidation of NCO. The DFT energy calculation results and microkinetic analyses revealed that the NCO generation step, possessing an energy barrier of 17.0 kcal mol-1 and a forward reaction rate constant of 2.20 × 107 s-1, was the rate-determining step of the whole catalytic cycle.

14.
Mater Sci Eng C Mater Biol Appl ; 57: 279-87, 2015 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-26354265

RESUMO

A highly sensitive electrochemical sensor for gallic acid (GA), an important polyphenolic compound, was fabricated using the hybrid material of chitosan (CS), fishbone-shaped Fe2O3 (fFe2O3), and electrochemically reduced graphene oxide (ERGO) as the sensing matrix. The electrochemical characterization experiments showed that the CS-fFe2O3-ERGO modified glassy carbon electrode (CS-fFe2O3-ERGO/GCE) had large surface area, excellent electronic conductivity and high stability. The GA presented a superior electrochemical response on CS-fFe2O3-ERGO/GCE in comparison with the single-component modified electrode. The electrochemical mechanism and optimal test conditions of GA on the electrode surface were carefully investigated. Under the optimal conditions, the oxidation peak currents in differential pulse voltammetry (DPV) experiments exhibited a good linear relationship with the logarithmic values of GA concentration over the range from 1.0×10(-6)M to 1.0×10(-4)M. Based on signal-to-noise (S/N) characteristic of 3, the detection limit was estimated to be 1.5×10(-7)M. The proposed sensor has also been applied for estimating the antioxidant capacity index of real samples of red and white wines.


Assuntos
Antioxidantes/análise , Condutometria/instrumentação , Compostos Férricos/química , Análise de Alimentos/instrumentação , Ácido Gálico/análise , Vinho/análise , Eletrodos , Galvanoplastia , Desenho de Equipamento , Análise de Falha de Equipamento , Grafite/química , Nanopartículas Metálicas/química , Nanopartículas Metálicas/ultraestrutura , Nanocompostos/química , Nanocompostos/ultraestrutura , Oxirredução
15.
Biosens Bioelectron ; 74: 447-53, 2015 Dec 15.
Artigo em Inglês | MEDLINE | ID: mdl-26164490

RESUMO

A versatile nanocomposite containing ß-cyclodextrin and graphene (CD-GR) was prepared through a simple chemical reduction method. The characterization experiments show that the nanocomposite remains the flake-like morphology of GR, but its solubility and stability in aqueous solution are greatly improved. Then the nanocomposite was modified at glassy carbon electrode (GCE) surface, and was used as a functional matrix for the covalent immobilization of probe DNA using 2,4,6-trichloro-1,3,5-triazine (TCT) as the crosslinker. Due to the synergetic effect of large surface area of GR and rich hydroxyl of CD, the probe density for the developed biosensor was determined to as high as 3.82×10(13) molecules cm(-2). Meanwhile, the biosensor shows high hybridization efficiency and hybridization kinetic. When the biosensor was applied for the impedance-based hybridization test, a wide linear range from 1.0×10(-16) to 1.0×10(-12) M and an ultralow detection limit of 3.4×10(-17) M were achieved. The biosensor also displays excellent stability, selectivity, and reproducibility.


Assuntos
Condutometria/instrumentação , DNA/química , DNA/genética , Grafite/química , Análise de Sequência de DNA/instrumentação , beta-Ciclodextrinas/química , Adsorção , Sequência de Bases , DNA/análise , Condutividade Elétrica , Eletrodos , Desenho de Equipamento , Análise de Falha de Equipamento , Hibridização In Situ/instrumentação , Dados de Sequência Molecular , Reprodutibilidade dos Testes , Sensibilidade e Especificidade
16.
Arthritis Rheumatol ; 67(1): 182-92, 2015 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-25307081

RESUMO

OBJECTIVE: To study the interactions between vascular endothelial cells and meniscal fibrochondrocytes from the inner avascular and outer vascular regions of the meniscus and to identify angiogenic factors that enhance cell migration and integrative repair. METHODS: Bovine meniscal fibrochondrocytes (bMFCs) from the inner and outer regions of meniscus were cultured for 7 days with or without human umbilical vein endothelial cells (HUVECs) in a micropatterned 3-dimensional hydrogel system for assessment of cell migration. Angiogenic factors secreted by HUVECs were probed for their role in paracrine mechanisms governing bMFC migration and applied to a full-thickness defect model of meniscal repair in explants from the inner and outer meniscal regions over 4 weeks. RESULTS: Endothelial cells enhanced the migration of inner and outer bMFCs in the micropatterned system via endothelin 1 (ET-1) signaling. Supplementation with ET-1 significantly enhanced the integration strength of full-thickness defects in the inner and outer explants, as well as cell migration at the macroscale level, as compared to controls without ET-1 treatment. CONCLUSION: This study is the first to show that bMFCs from both the avascular and vascular regions of the meniscus respond to the presence of endothelial cells with increased migration. Paracrine signaling by endothelial cells regulates the bMFCs differentially by region, but we identified ET-1 as an angiogenic factor that stimulates the migration of inner and outer cells at the microscale level and the integrative repair of inner and outer explants at the macroscale level. These findings reveal the regional interactions between the vasculature and MFCs, and suggest ET-1 as a potential new treatment for avascular meniscus injuries in order to prevent the development of osteoarthritis.


Assuntos
Comunicação Celular/fisiologia , Movimento Celular/fisiologia , Condrócitos/fisiologia , Células Endoteliais/fisiologia , Meniscos Tibiais/fisiologia , Animais , Bovinos , Células Cultivadas , Condrócitos/citologia , Técnicas de Cocultura , Células Endoteliais/citologia , Endotelina-1/fisiologia , Humanos , Meniscos Tibiais/citologia , Modelos Animais , Neovascularização Fisiológica/fisiologia , Comunicação Parácrina/fisiologia , Transdução de Sinais/fisiologia
17.
Sci Rep ; 4: 3674, 2014 Jan 14.
Artigo em Inglês | MEDLINE | ID: mdl-24419206

RESUMO

Electrical signals have been applied towards the repair of articular tissues in the laboratory and clinical settings for over seventy years. We focus on healing of the meniscus, a tissue essential to knee function with limited innate repair potential, which has been largely unexplored in the context of electrical stimulation. Here we demonstrate for the first time that electrical stimulation enhances meniscus cell migration and integrative tissue repair. We optimize pulsatile direct current electrical stimulation parameters on cells at the micro-scale, and apply these to healing of full-thickness defects in explants at the macro-scale. We report increased expression of the adenosine A2b receptor in meniscus cells after stimulation at the micro- and macro-scale, and propose a role for A2bR in meniscus electrotransduction. Taken together, these findings advance our understanding of the effects of electrical signals and their mechanisms of action, and contribute to developing electrotherapeutic strategies for meniscus repair.


Assuntos
Movimento Celular , Estimulação Elétrica , Regeneração Tecidual Guiada/métodos , Lesões do Menisco Tibial , Cicatrização , Animais , Bovinos , Técnicas de Cocultura , Células Endoteliais da Veia Umbilical Humana , Humanos , Modelos Biológicos , Receptor A2B de Adenosina/metabolismo
18.
Zhongguo Wei Zhong Bing Ji Jiu Yi Xue ; 23(11): 681-4, 2011 Nov.
Artigo em Chinês | MEDLINE | ID: mdl-22093315

RESUMO

OBJECTIVE: To understand the situation of the device-associated infection (DAI) in the medical-surgical intensive care unit(ICU)inpatients in an A-level tertiary class hospital in Beijing. METHODS: DAI date were collected through a surveillance on the medical-surgical ICU inpatients in an A-level tertiary class hospital in Beijing from January 2008 to December 2010. RESULTS: In 2279 patients admitted to the medical-surgical ICU (with a 15,332 days total hospitalization stay), 283 were found infected. The incidence for in-hospital infection was 12.42%, and 2.452% for the incidence per patient-day. The device utilization ratios for ventilator, central venous catheter and urinary catheter were 56.76%, 59.01% and 80.07% respectively while the incidence for ventilator-associated pneumonia (VAP), central line-associated bloodstream infection (CLABSI) and catheter-associated urinary tract infection (CAUTI) were 1.632%, 0.409% and 0.350% respectively. The predominant bacteria species found in these cases were Gram-negatives and the main stay of pathogenic species were A. baumannii, P. aeruginosa, Staphylococcus, E. coli, K. pneumoniae and C. albicans etc. CONCLUSION: The incidence of DAI in the surveyed hospital is close to other hospitals in China and other developing countries but higher than hospitals in United States. More efforts should be made for its prevention / control by hospital stuff, with the cooperation from the patients.


Assuntos
Infecção Hospitalar/epidemiologia , Infecção Hospitalar/prevenção & controle , Equipamentos e Provisões/efeitos adversos , Pacientes Internados , Cateterismo Venoso Central/efeitos adversos , Cateteres de Demora/efeitos adversos , Cateteres de Demora/microbiologia , China , Contaminação de Equipamentos , Equipamentos e Provisões/microbiologia , Humanos , Incidência , Unidades de Terapia Intensiva , Pneumonia Associada à Ventilação Mecânica/epidemiologia , Pneumonia Associada à Ventilação Mecânica/prevenção & controle , Respiração Artificial/efeitos adversos , Infecções Urinárias/epidemiologia , Infecções Urinárias/prevenção & controle
19.
Anat Rec (Hoboken) ; 290(1): 48-58, 2007 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-17441197

RESUMO

The knee menisci are wedge-shaped semilunar fibrocartilaginous structures that reside between the femur and tibia and function to transmit and distribute load. These structures have characteristics of both fibrous and cartilaginous tissues. The cartilage-like inner region and the fibrous vascularized outer region each has a distinct extracellular matrix, and resident meniscal fibrochondrocytes (MFCs) with distinct morphologies dependent on their location. Damage to the meniscus is common, and disruption of tissue structure and function result in erosion of the underlying articular cartilage. It has been observed that damage in the vascular periphery undergoes spontaneous repair, whereas damage of the inner region does not heal. While vascularity of the peripheral region plays a role in healing, recent findings have also suggested that local cellular composition influences local healing capacity. This study examined the variation in multipotential characteristics of cell populations isolated from different regions of the bovine meniscus. MFCs were isolated from the outer (vascular), inner (avascular), and horn (mixed) regions and induced toward chondrogenic, adipogenic, and osteogenic lineages. The results of this study suggest that MFCs from all regions of the meniscus possess a multilineage differentiation capability, particularly toward chondrogenesis and adipogenesis. MFCs from the outer region were most plastic, differentiating along all three mesenchymal lineages. These findings may underlie the experimental observation of improved integration of meniscus grafts from the outer zone and may have implications for developing strategies of cell-based meniscus repair.


Assuntos
Diferenciação Celular/fisiologia , Linhagem da Célula/fisiologia , Condrócitos/citologia , Meniscos Tibiais/citologia , Meniscos Tibiais/fisiologia , Adipogenia/fisiologia , Animais , Bovinos , Células Cultivadas , Condrócitos/fisiologia , Condrogênese/fisiologia , Consolidação da Fratura/fisiologia , Humanos , Osteogênese/fisiologia , Regeneração/fisiologia
20.
J Immunol ; 178(3): 1450-6, 2007 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-17237393

RESUMO

F2L (formylpeptide receptor (FPR)-like (FPRL)-2 ligand), a highly conserved acetylated peptide derived from the amino-terminal cleavage of heme-binding protein, is a potent chemoattractant for human monocytes and dendritic cells, and inhibits LPS-induced human dendritic cell maturation. We recently reported that F2L is able to activate the human receptors FPRL-1 and FPRL2, two members of the FPR family, with highest selectivity and affinity for FPRL2. To facilitate delineation of mechanisms of F2L action in vivo, we have now attempted to define its mouse receptors. This is complicated by the nonequivalence of the human and mouse FPR gene families (three vs at least eight members, respectively). When cell lines were transfected with plasmids encoding the eight mouse receptors, only the one expressing the receptor Fpr2 responded to F2L (EC(50) approximately 400 nM for both human and mouse F2L in both calcium flux and cAMP inhibition assays). This value is similar to F2L potency at human FPRL1. Consistent with this, mouse neutrophils, which like macrophages and dendritic cells express Fpr2, responded to human and mouse F2L in both calcium flux and chemotaxis assays with EC(50) values similar to those found for Fpr2-expressing cell lines ( approximately 500 nM). Moreover, neutrophils from mice genetically deficient in Fpr2 failed to respond to F2L. Thus, Fpr2 is a mouse receptor for F2L, and can be targeted for the study of F2L action in mouse models.


Assuntos
Fatores Quimiotáticos/fisiologia , Neutrófilos/fisiologia , Receptores de Formil Peptídeo/metabolismo , Animais , Cálcio , Proteínas de Transporte , Quimiotaxia , Proteínas Ligantes de Grupo Heme , Hemeproteínas , Humanos , Camundongos , Peptídeos
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