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1.
Zhonghua Wai Ke Za Zhi ; 62(6): 606-612, 2024 Jun 01.
Artigo em Chinês | MEDLINE | ID: mdl-38682633

RESUMO

Objective: To explore the risk factors of short-term prognosis of severe Budd-Chiari syndrome (BCS) patients,established and verified the nomogram prediction model for these BCS patients and evaluated its clinical application value. Methods: This study is a retrospective cohort study. The clinical data of 171 patients with severe BCS diagnosed were retrospectively analyzed in the Department of Hepatopancreatobiliary Surgery First Affiliated Hospital of Zhengzhou University from January 2018 to December 2023. There were 105 males and 66 females, aged (52.1±12.8) years (range: 18 to 79 years). The patients were divided into two groups based on whether they died within 28 days: the death group (n=38) and the survival group (n=133). The risk factors for short-term death of patients were analyzed,and independent risk factors were screened by univariate and multivariate analysis. Furthermore,these factors were used to establish the nomogram prediction model. The area under the curve(AUC),the Bootstrap Resampling,the Hosmer-Lemeshow test and the Decision Curve Analysis(DCA) were used to verify the model's differentiation,internal verification,calibration degree and clinical effectiveness,respectively. Results: Univariate and multivariate Logistics regression analysis showed that the history of hepatic encephalopathy,white blood cell,glomerular filtration rate and prothrombin time were independent risk factors (P<0.05). The above factors were used to successfully establish the prediction model with 0.908 of AUC and 0.895 of the internal verification of AUC,indicating that the predictive model was valuable. The 0.663 P-values in the Hosmer-Lemeshow test indicated the high calibration degree of the model. The clinical effectiveness of the model was proved by the 18% clinical benefit population using the DCA curve with the 17% probability threshold. Conclusions: The independent risk factors are the history of hepatic encephalopathy,white blood cell,glomerular filtration rate and prothrombin time. An adequate basis was acquired by establishing a nomogram prediction model of the short-term prognosis of severe BCS,which was helpful for early clinical screening and identification of high-risk patients with severe BCS who could die in the short term and timely providing timely intervention measures for improving the prognosis.


Assuntos
Síndrome de Budd-Chiari , Nomogramas , Humanos , Feminino , Masculino , Pessoa de Meia-Idade , Síndrome de Budd-Chiari/diagnóstico , Síndrome de Budd-Chiari/cirurgia , Estudos Retrospectivos , Prognóstico , Fatores de Risco , Adulto , Idoso , Adolescente , Adulto Jovem
2.
Cell Mol Biol (Noisy-le-grand) ; 58 Suppl: OL1803-8, 2012 Dec 05.
Artigo em Inglês | MEDLINE | ID: mdl-23217440

RESUMO

The Ubiquitin--specific protease 22 (USP22) is a new putative cancer stem cell marker, which plays a significant role in tumorigenesis and cell--cycle progression. However, little is known about the impact of USP22 knock--down on the growth of human hepatoma cell lines. In this study, elevated expression of USP22 was observed in the human HepG2 hepatic cancer cell line compared to the normal human hepatocyte Chang liver cell line. Subsequently, we used siRNA specifically suppressing expression of USP22 and observed that the knock--down of USP22 could effectively induce cell cycle arrest and inhibit HepG2 cell proliferation. Furthermore, our results showed that USP22 deletion caused down--regulation of cyclin D2 expression and up--regulation of p15 and p21 expression. Collectively, Our findings indicate that USP22 may be responsible for HepG2 cell growth and USP22 regulates the cell cycle via the c--Myc/cyclin D2 pathway and down--regulating p15 and p21 expression in HepG2 cell.


Assuntos
RNA Interferente Pequeno/metabolismo , Tioléster Hidrolases/antagonistas & inibidores , Pontos de Checagem do Ciclo Celular , Linhagem Celular , Proliferação de Células , Ciclina D2/metabolismo , Inibidor de Quinase Dependente de Ciclina p15/metabolismo , Inibidor de Quinase Dependente de Ciclina p21/metabolismo , Células Hep G2 , Humanos , Proteínas Proto-Oncogênicas c-myc/metabolismo , Interferência de RNA , Transdução de Sinais , Tioléster Hidrolases/genética , Tioléster Hidrolases/metabolismo , Ubiquitina Tiolesterase , Regulação para Cima
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