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Chromodomain helicase DNA binding protein 5 (CHD5) was previously proposed to function as a potent tumor suppressor by acting as a master regulator of a tumor-suppressive network. CHD5 is down-regulated in several cancers, including leukemia and is responsible for tumor generation and progression. However, the mechanism of CHD5 down-regulation in leukemia is largely unknown. In this study, quantitative reverse-transcriptase polymerase chain reaction and western blotting analyses revealed that CHD5 was down-regulated in human leukemia cell lines and samples. Luciferase reporter assays showed that most of the baseline regulatory activity was localized from 500 to 200 bp upstream of the transcription start site. Bisulfite DNA sequencing of the identified regulatory element revealed that the CHD5 promoter was hypermethylated in human leukemia cells and samples. Thus, CHD5 expression was inversely correlated with promoter DNA methylation in these samples. Treatment with DNA methyltransferase inhibitor 5-aza-2′-deoxycytidine (DAC) activates CHD5 expression in human leukemia cell lines. In vitro luciferase reporter assays demonstrated that methylation of the CHD5 promoter repressed its promoter activity. Furthermore, a chromatin immunoprecipitation assay combined with qualitative PCR identified activating protein 2 (AP2) as a potential transcription factor involved in CHD5 expression and indicated that treatment with DAC increases the recruitment of AP2 to the CHD5 promoter. In vitro transcription-factor activity studies showed that AP2 over-expression was able to activate CHD5 promoter activity. Our findings indicate that repression of CHD5 gene expression in human leukemia is mediated in part by DNA methylation of its promoter. [ABSTRACT FROM AUTHOR]

Facing the pressure of environment, sustainable development is the demand of the current construction industry development. Prefabricated construction technologies has been actively promoted in China. Cost has always been one of the important factors in the development of prefabricated buildings. The hidden cost of prefabricated buildings has a great impact on the total cost of the project, and it exists in the whole process of building construction. In this paper innovatively studies the cost of prefabricated buildings from the perspective of hidden cost. In order to analysis the hidden cost of prefabricated buildings, the influencing factor index system in terms of design, management, technology, policy and environment has been established, which includes 13 factors in total. And the hidden cost analysis model has been proposed based on FISM-BN, this model combines fuzzy interpretive structure model(FISM) with Bayesian network(BN). This model can comprehensively analyze the hidden cost through the combination of qualitative and quantitative methods. And the analysis process is dynamic, not fixed at a certain point in time to analyze the cost. We can get the internal logical relationship among the influencing factors of the hidden cost, and present it in the form of intuitive chart by FISM-BN. Furthermore the model could not only predict the probability of the hidden cost of prefabricated buildings and realize in-time control through causal reasoning, but also predict the posterior probability of other influencing factors through diagnostic reasoning when the hidden cost occurs and find out the key factors that lead to the hidden cost. Then the final influencing factors are determined after one by one check. Finally, the model is demonstrated on the hidden cost analysis of prefabricated buildings the probability of recessive cost is 26%. In the analysis and control of the hidden cost of prefabricated buildings, scientific and effective decision-making and reference opinions are provided for managers. [ABSTRACT FROM AUTHOR]

Numerous factors impact on the prognosis of acute myeloid leukemia (AML), among which molecular genetic abnormalities are developed increasingly, however, accurate prediction for newly diagnosed AML patients remains unsatisfied. For further improving the prognosis evaluation system, we investigated the transcripts levels of PDCD7, FIS1, FAM3A, CA6, APP, KLRF1, ATCAY, GGT5 and Ang2 in 97 AML patients and 30 non-malignant controls, and validated using the published microarray data from 225 cytogenetically normal AML (CN-AML) patients treated according to the German AMLCG-1999 protocol. Real-time quantitative polymerase chain reaction and western blot were carried out, and clinical data were collected and analyzed. High Ang2 and FIS1 expression discriminated the CR rate of AML patients (62.5% versus 82.9% for Ang2, P = 0.011; 61.4% versus 82.2% for FIS1, P = 0.029). In CN-AML, patients with high FIS1 expression were more likely to be resistant to two courses of induction (P = 0.035). Overall survival (OS) and relapse-free survival (RFS) were shorter in CN-AML patients with high PDCD7 expression (P<0.001; P = 0.006), and PDCD7 was revealed to be an independent risk factor for OS in CN-AML (P = 0.004). In the analysis of published data from 225 CN-AML patients, PDCD7 remained independently predicting OS in CN-AML (P = 0.039). As a conclusion, Ang2 and FIS1 seem related to decreased CR rate of AML patients, and PDCD7 is associated with shorter OS and RFS in CN-AML. Hence, PDCD7, Ang2 and FIS1 may indicate a more aggressive form and poor prognosis of AML. [ABSTRACT FROM AUTHOR]