RESUMO
Objective To analyze the trends of disease burden of cervical cancer,uterine cancer,and ovarian cancer among Chinese women from 1990 to 2019,and to provide a basis for formulating precise prevention and control measures in China. Methods The global disease burden data in 2019 were used to describe the changes in indicators such as incidence,mortality,years of life lost due to premature mortality(YLL),years lived with disability(YLD),and disability-adjusted life year(DALY) of cervical,uterine,and ovarian cancers in China from 1990 to 2019.Furthermore,the Bayesian age-period-cohort model was adopted to predict the incidence and mortality of the cancers from 2020 to 2030. Results From 1990 to 2019,the incidence rates and mortality of cervical,uterine,and ovarian cancers in Chinese women showed an upward trend,and the age-standardized incidence rate of ovarian cancer increased the most(0.78%).In 2019,the incidence of cervical cancer and uterine cancer concentrated in the women of 55-59 years old,and ovarian cancer mainly occurred in the women of 70-74 years old.The DALY,YLL,and YLD of cervical,uterine,and ovarian cancers all presented varying degrees of growth at all ages.The Bayesian age-period-cohort model predicted that from 2020 to 2030,the incidence and mortality of cervical cancer in China showed a decreasing trend,while those of uterine cancer and ovarian cancer showed an increasing trend.There was no significant change in the age with high incidence of the three cancers. Conclusions From 1990 to 2019,the overall disease burden of cervical,uterine,and ovarian cancers in China increased,while the disease burden of cervical cancer decreased after 2020.It is recommended that the efforts should be doubled for the prevention and control of cervical,uterine,and ovarian cancers.
Assuntos
Neoplasias Ovarianas , Neoplasias do Colo do Útero , Feminino , Humanos , Pessoa de Meia-Idade , Idoso , Neoplasias do Colo do Útero/epidemiologia , Teorema de Bayes , Neoplasias Ovarianas/epidemiologia , Efeitos Psicossociais da Doença , Genitália , China/epidemiologiaRESUMO
Objective To investigate the relationship between the expression of glutathione peroxidase(GPX)genes and the clinical prognosis in glioma patients,and to construct and evaluate the model for predicting the prognosis of glioma. Methods The clinical information and GPX expression of 663 patients,including 153 patients of glioblastoma(GBM)and 510 patients of low-grade glioma(LGG),were obtained from The Cancer Genome Atlas(TCGA)database.The relationship between GPX expression and patient survival was analyzed.The key GPX affecting the prognosis of glioma was screened out by single- and multi-factor Cox's proportional-hazards regression models and validated by least absolute shrinkage and selection operator(Lasso)regression.Finally,we constructed the model for predicting the prognosis of glioma with the screening results and then used concordance index and calibration curve respectively to evaluate the discrimination and calibration of model. Results Compared with those in the control group,the expression levels of GPX1,GPX3,GPX4,GPX7,and GPX8 were up-regulated in glioma patients(all P<0.001).Moreover,the expression levels of other GPX except GPX3 were higher in GBM patients than in LGG patients(all P<0.001).The Kaplan-Meier curves showed that the progression-free survival of GBM with high expression of GPX1(P=0.013)and GPX4(P=0.040),as well as the overall survival,disease-specific survival,and progression-free survival of LGG with high expression of GPX1,GPX7,and GPX8,was shortened(all P<0.001).GPX7 and GPX8 were screened out as the key factors affecting the prognosis of LGG.The results were further used to construct a nomogram model,which suggested GPX7 was the most important variable.The concordance index of the model was 0.843(95%CI=0.809-0.853),and the calibration curve showed that the predicted and actual results had good consistency. Conclusion GPX7 is an independent risk factor affecting the prognosis of LGG,and the nomogram model constructed with it can be used to predict the survival rate of LGG.
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Neoplasias Encefálicas , Glioblastoma , Glioma , Glioma/diagnóstico , Glutationa Peroxidase/metabolismo , Humanos , Peroxidases , Prognóstico , Modelos de Riscos ProporcionaisRESUMO
Objective To study the gene expression of cardiac mesenchymal cells in patients with type 2 diabetes mellitus (T2DM)based on a whole-genome high-throughput sequencing dataset,screen differentially expressed genes,analyze the genetics signature of cardiac mesenchymal cells in T2DM patients by bioinformatics analysis,and explore the environmental chemicals related to the key differentially expressed genes. Methods The dataset GSE106177 was obtained from Gene Expression Omnibus (GEO) database.The dataset was pre-processed and analyzed by Network Analyst,Cytoscape 3.7.1,String11.0,CTD,and HMDD for screening for differentially expressed genes,enrichment analysis,establishment of protein-protein interaction (PPI) networks,and screening for relevant environmental chemicals. Results The gene expression pattern of cardiac mesenchymal cells in T2DM patients was significantly different from that in the control group.There were 135 differentially expressed genes,of which 58 (42.96%) were up-regulated and 77 (57.04%) were down-regulated.The differentially expressed genes mainly participated in biological processes such as multicellular organism development,anatomical structure development,and system development and were mainly involved in hepatocellular carcinoma,Cushing's syndrome,and cholesterol metabolism.PPI network showed that UBC was the core protein node.The microRNA-Gene interaction network showed that seven microRNAs,represented by hsa-mir-8485,interacted with the differentially expressed genes.Key T2DM related genes such as UBC,DNER,and CNTN1 interacted with bisphenol A. Conclusions The gene expression profile of cardiac mesenchymal cells markedly changes in T2DM patients,during which UBC may play an important biological role.Bisphenol A exposure may also affect the development and normal function of cardiac cells in T2DM patients.
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Diabetes Mellitus Tipo 2/metabolismo , Células-Tronco Mesenquimais/metabolismo , MicroRNAs/genética , Miocárdio/citologia , Transcriptoma , Biologia Computacional , Perfilação da Expressão Gênica , HumanosRESUMO
Objective To analyze the differentially expressed genes and key proteins in T cells between acute and chronic idiopathic thrombocytopenic purpura (ITP) in children and provide the basis for the prevention and therapies of this disease. Methods Microarray gene chip data from T cells of children with acute or chronic ITP were downloaded from the GEO Database. The gene expression profiles,gene function,and protein interaction network were analyzed by R,QOE,Networkanalyst,GCBI,and GenClip. Results The gene expression profiles between these two groups were significantly different. Among the 54 675 genes analyzed,there were 457 (0.84%) differentially expressed genes between these two groups. In the protein interaction networks among top 20 differentially expressed genes,the core was JUN(down-regulated) and ITCH(up-regulated),which were both related to the tumor necrosis factor signaling pathway;differentially expressed genes were mainly related to the activation and tolerance of T cell. Conclusions The gene expression profiles differ between acute and chronic ITP patients,suggesting that the gene transcription profile plays a regulatory role in the different stages of ITP. JUN and ITCH may play a role in predict the progression of ITP and may exert their biological functions by regulating the tumor necrosis factor signaling pathway.
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Púrpura Trombocitopênica Idiopática/genética , Transcriptoma , Doença Aguda , Criança , Doença Crônica , Humanos , Análise de Sequência com Séries de Oligonucleotídeos , Púrpura Trombocitopênica Idiopática/classificação , Linfócitos TRESUMO
BACKGROUND: The long-term effects of bone marrow-derived cells (BMC) transplantation in patients with acute myocardial infarction (AMI) have not been established. The present meta-analysis of randomized controlled trials with follow-up ≥ 2 years was performed to investigate the long-term effects of BMC therapy in patients after AMI. METHODS: Specific terms were used to conduct a systematic literature search of MEDLINE, EMBASE, the Cochrane Library and the Cochrane Central Register of Controlled Trials, and the China Biological Medicine Disk database from their inception to March 2012. A standardized protocol was used to extract information, and random effect model was used to analyze all data except major adverse events. RESULTS: Five trials comprising 510 patients were included. Compared with controls, BMC therapy significantly improved left ventricular ejection fraction (LVEF) (4.18%, 95%CI: 2.02% to 6.35%, P = 0.0002), while mildly but not significantly reduced left ventricular end-systolic volume (-4.47 ml, 95%CI: -10.92 to 1.99, P = 0.17) and left ventricular end-diastolic volume (-2.29 ml, 95%CI: -9.96 to 5.39, P = 0.56). Subgroup analysis revealed that significant improvement of LVEF induced by BMC therapy could be observed in patients with baseline LVEF ≤ 42%, but disappeared in those with baseline LVEF > 42%. There were trends in favor of BMC therapy for most major clinical adverse events, though most differences were not significant. CONCLUSIONS: Intracoronary BMC infusion in patients with AMI seems to be safe and may further improve LVEF on top of standard therapy; especially the beneficial effects could last for long term. The findings need to be validated in the future.