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1.
IUBMB Life ; 72(11): 2469-2480, 2020 11.
Artigo em Inglês | MEDLINE | ID: mdl-32959533

RESUMO

Long noncoding RNA SOX2OT is associated with myocardial fibrosis (MF) in heart failure (HF). This article aims to investigate the role of SOX2OT in MF. We constructed HF mouse models by subcutaneous injection of isoprenaline (ISO). Cardiac fibroblasts (CFs) were treated with ISO to induce MF.Hematoxylin-eosin, Masson, and Sirius-red staining were used to identify myocardial injury and collagen deposition in heart tissues. The relationship among SOX2OT, miR-138-5p, TGF-ß1, and Smad3 were evaluated by chromatin immunoprecipitation and luciferase reporter assay. The gene and protein expression were verified by quantitative real-time PCR and western blot. We found that SOX2OT was up-regulated in HF mice and ISO-induced CFs. SOX2OT knockdown reduced myocardial injury and collagen deposition in HF mice. The expression of collagen I, α-SMA, TGF-ß1, and p-Smad3 were inhibited by SOX2OT down-regulation in HF mice and ISO-induced CFs. Furthermore, TGF-ß1 was a target gene of miR-138-5p and indirectly regulated by SOX2OT. SOX2OT promoted MF in HF by activating TGF-ß1/Smad3, and then Smad3 interacted with the SOX2OT promoter and formed a positive feedback loop. In conclusion, our work verifies that SOX2OT/Smad3 feedback loop promotes MF in HF. Thus, SOX2OT is potentially a novel therapeutic target for MF in HF.


Assuntos
Cardiomiopatias/patologia , Fibrose/patologia , Insuficiência Cardíaca/complicações , MicroRNAs/genética , RNA Longo não Codificante/genética , Proteína Smad3/metabolismo , Fator de Crescimento Transformador beta1/metabolismo , Animais , Cardiomiopatias/etiologia , Cardiomiopatias/metabolismo , Proliferação de Células , Retroalimentação , Fibrose/etiologia , Fibrose/metabolismo , Regulação da Expressão Gênica , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Proteína Smad3/genética , Fator de Crescimento Transformador beta1/genética
2.
Sensors (Basel) ; 17(10)2017 Sep 21.
Artigo em Inglês | MEDLINE | ID: mdl-28934159

RESUMO

A Pervasive-computing-enriched smart home environment, which contains many embedded and tiny intelligent devices and sensors coordinated by service management mechanisms, is capable of anticipating intentions of occupants and providing appropriate services accordingly. Although there are a wealth of research achievements in recent years, the degree of market acceptance is still low. The main reason is that most of the devices and services in such environments depend on particular platform or technology, making it hard to develop an application by composing the devices or services. Meanwhile, the concept of Web of Things (WoT) is becoming popular recently. Based on WoT, the developers can build applications based on popular web tools or technologies. Consequently, the objective of this paper is to propose a set of novel WoT-driven plug-and-play service management schemes for a smart home called Resource-Oriented Service Administration (ROSA). We have implemented an application prototype, and experiments are performed to show the effectiveness of the proposed approach. The results of this research can be a foundation for realizing the vision of "end user programmable smart environments".

3.
J Clin Transl Hepatol ; 11(1): 97-109, 2023 Feb 28.
Artigo em Inglês | MEDLINE | ID: mdl-36406327

RESUMO

Background and Aims: The goal of this study was to investigate the mechanism by which the long noncoding RNA MALAT1 inhibited hepatocyte proliferation in acute liver injury (ALI). Methods: Lipopolysaccharide (LPS) was used to induce an ALI cellular model in HL7702 cells, in which lentivirus vectors containing MALAT1/EZH2/GFER overexpression or knockdown were introduced. A series of experiments were performed to determine their roles in liver injury, oxidative stress injury, and cell biological processes. The interaction of MALAT1 with EZH2 and enrichment of EZH2 and H3K27me3 in the GFER promoter region were identified. Rats were treated with MALAT1 knockdown or GFER overexpression before LPS induction to verify the results derived from the in vitro assay. Results: MALAT1 levels were elevated and GFER levels were reduced in ALI patients and the LPS-induced cell model. MALAT1 knockdown or GFER overexpression suppressed cell apoptosis and oxidative stress injury induced cell proliferation, and reduced ALI. Functionally, MALAT1 interacted directly with EZH2 and increased the enrichment of EZH2 and H3K27me3 in the GFER promoter region to reduce GFER expression. Moreover, MALAT1/EZH2/GFER was activated the AMPK/mTOR signaling pathway. Conclusion: Our study highlighted the inhibitory role of reduced MALAT1 in ALI through the modulation of EZH2-mediated GFER.

4.
J Clin Neurosci ; 99: 147-151, 2022 May.
Artigo em Inglês | MEDLINE | ID: mdl-35279587

RESUMO

INTRODUCTION: The efficacy of yoga therapy for migraine remains controversial. We conduct this meta-analysis to explore the influence of yoga therapy on the treatment efficacy of migraine. METHODS: We have searched PubMed, EMbase, Web of science, EBSCO and Cochrane library databases through February 2021, and included randomized controlled trials (RCTs) assessing the efficacy of yoga therapy for migraine attack. RESULTS: Five RCTs involving 356 patients were included in the meta-analysis. Overall, compared with control group for migraine, yoga therapy was associated with substantially reduced headache frequency headache frequency (SMD = -1.43; 95% CI = -2.23 to -0.64; P = 0.0004) and HIT-6 score (SMD = -2.19; 95% CI = -4.09 to -0.28; P = 0.02), but revealed no obvious influence on pain intensity (SMD = -1.37; 95% CI = -2.76 to 0.01; P = 0.05) or McGill Pain Questionnaire (SMD = -2.09; 95% CI = -6.39 to 2.22; P = 0.34). CONCLUSIONS: Yoga therapy may benefit to reduce the headache frequency of migraine patients.


Assuntos
Transtornos de Enxaqueca , Yoga , Cefaleia , Humanos , Transtornos de Enxaqueca/terapia , Medição da Dor , Ensaios Clínicos Controlados Aleatórios como Assunto , Resultado do Tratamento
5.
Comput Math Methods Med ; 2022: 6161015, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35844461

RESUMO

This research was aimed at exploring the changes in right ventricular function in patients after the recovery of coronavirus disease 2019 (COVID-19) under echocardiography and providing a reference for the rehabilitation and treatment of COVID-19 patients. Three echocardiographic follow-up examinations were performed on 40 recovered COVID-19 patients and 40 healthy people. Right ventricular function between patients after COVID-19 rehabilitation and healthy people was compared. The mean values of right ventricular fractional area change (RVFAC), tricuspid annular plane systolic excursion (TAPSE), right ventricular ejection fraction (RVEF), right myocardial performance index (RMPI), and tricuspid annular plane systolic speed (S') were compared between patients after COVID-19 rehabilitation and healthy subjects. The technical parameters of two-dimensional speckle tracking were compared. The results showed that the differences in RVFAC, TAPSE, RVEF, and RMPI between COVID-19 patients and healthy controls were not significant during the three follow-up periods (P > 0.05). At the first follow-up, the S' was 12.78 cm/s in COVID-19 patients and 13.18 cm/s in healthy subjects. At the second follow-up, the S' was 11.98 cm/s in COVID-19 patients and 12.77 cm/s in healthy subjects. At the third follow-up, the S' was 12.79 cm/s in COVID-19 patients and 13.12 cm/s in healthy subjects. There was no significant difference between the two groups (P > 0.05). In addition, there was no significant difference in right ventricular function between COVID-19 patients and healthy controls, and there was no significant difference in cardiovascular symptoms (P > 0.05). In summary, COVID-19 had no substantial effect on right ventricular function and better recovery in patients.


Assuntos
COVID-19 , Disfunção Ventricular Direita , COVID-19/diagnóstico por imagem , Ecocardiografia , Humanos , Volume Sistólico , Disfunção Ventricular Direita/diagnóstico por imagem , Disfunção Ventricular Direita/etiologia , Função Ventricular Direita
6.
PeerJ ; 10: e12731, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-35178291

RESUMO

BACKGROUND: Identification of accurate prognostic biomarkers is still particularly urgent for improving the poor survival of lung cancer patients. In this study, we aimed to identity the potential biomarkers in Chinese lung cancer population via bioinformatics analysis. METHODS: In this study, the differentially expressed genes (DEGs) in lung cancer were identified using six datasets from Gene Expression Omnibus (GEO) database. Subsequently, enrichment analysis was conducted to evaluate the underlying molecular mechanisms involved in progression of lung cancer. Protein-protein interaction (PPI) and CytoHubba analysis were performed to determine the hub genes. The GEPIA, Human Protein Atlas (HPA), Kaplan-Meier plotter, and TIMER databases were used to explore the hub genes. The receiver operating characteristic (ROC) analysis was performed to evaluate the diagnostic value of hub genes. Reverse transcription quantitative PCR (qRT-PCR) was used to validate the expression levels of hub genes in 10 pairs of lung cancer paired tissues. RESULTS: A total of 499 overlapping DEGs (160 upregulated and 339 downregulated genes) were identified in the microarray datasets. DEGs were mainly associated with pathways in cancer, focal adhesion, and protein digestion and absorption. There were nine hub genes (CDKN3, MKI67, CEP55, SPAG5, AURKA, TOP2A, UBE2C, CHEK1 and BIRC5) identified by PPI and module analysis. In GEPIA database, the expression levels of these genes in lung cancer tissues were significantly upregulated compared with normal lung tissues. The results of prognostic analysis showed that relatively higher expression of hub genes was associated with poor prognosis of lung cancer. In HPA database, most hub genes were highly expressed in lung cancer tissues. The hub genes have good diagnostic efficiency in lung cancer and normal tissues. The expression of any hub gene was associated with the infiltration of at least two immune cells. qRT-PCR confirmed that the expression level of CDKN3, MKI67, CEP55, SPAG5, AURKA, TOP2A were highly expressed in lung cancer tissues. CONCLUSIONS: The hub genes and functional pathways identified in this study may contribute to understand the molecular mechanisms of lung cancer. Our findings may provide new therapeutic targets for lung cancer patients.


Assuntos
Perfilação da Expressão Gênica , Neoplasias Pulmonares , Humanos , Perfilação da Expressão Gênica/métodos , Aurora Quinase A/genética , População do Leste Asiático , Biomarcadores Tumorais/genética , Neoplasias Pulmonares/genética , Biologia Computacional/métodos , Proteínas de Ciclo Celular/genética
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