Optimizing the Diameter of Plugging Balls in Deep Shale Gas Wells

Deep shale gas reserves that have been fractured typically have many relatively close perforation holes. Due to theproximity of each fracture during the formation of the fracture network, there is significant stress interference,which results in uneven fracture propagation. It is common practice to use “balls” to temporarily plug fractureopenings in order to lessen liquid intake and achieve uniform propagation in each cluster. In this study, a diameteroptimization model is introduced for these plugging balls based on a multi-cluster fracture propagationmodel and a perforation dynamic abrasion model. This approach relies on proper consideration of the multiphasenature of the considered problem and the interaction force between the involved fluid and solid phases. Accordingly,it can take into account the behavior of the gradually changing hole diameter due to proppant continuousperforation erosion. Moreover, it can provide useful information about the fluid-dynamic behavior of the consideredsystem before and after plugging. It is shown that when the diameter of the temporary plugging ball is1.2 times that of the perforation hole, the perforation holes of each cluster can be effectively blocked.

KLF1和KLF9对K562细胞红系分化的协同调控作用

Krüppel样因子(Krüppel-like factors,KLFs)是锌指蛋白超家族的一个亚家族,参与细胞内的多种生理、病理过程,该家族成员在红细胞分化发育过程中发挥非常重要的作用,但是家族成员间对红系分化的协同调控作用还鲜有报道。本课题组前期研究发现,KIF家族成员KLF1和KLF9在已分化的红系细胞中的表达水平显著高于造血干细胞。为进一步探讨二者在红系分化中是否存在协同作用,本研究在K562细胞中分别过表达/敲低表达KLF1和KLF9,检测二者表达的相关性,发现KLF1和KLF9的基因表达呈现正相关,且二者共表达可以显著促进K562细胞红系分化,特异地增强β-珠蛋白的表达。通过对KLF1、KLF9单独和共同过表达、敲低表达的K562细胞转录组数据的分析发现二者可能通过PI3K-Akt和FoxO通路协同调控红系分化,FOS、TF、IL8是协同调控的候选靶基因。本研究结果为后续深入研究KLF1和KLF9协同调控红系分化的分子机制奠定了基础。

Failure pressure calculation of fracturing well based on fluid-structure interaction

Failure pressure is a key parameter in reservoir hydrofracturing operation. Existing analytical methods for calculating the failure pressure are based on the assumption that borehole fluid is under two extreme conditions: non-infiltration or complete infiltration. The assumption is not suitable for the actual infiltration process, and this will cause a great error in practical calculation. It shows that during the injection process, the dynamic variation in effective stress-dependent permeability has an influence on the infiltration, and the influence also brings about calculation errors. Based on the fluid-structure interaction and finite element method (FEM), considering partial infiltration during injection process, a numerical model for calculating rock failure pressure is established. According to the analysis of permeability test results and response-surface method, a new variation rule of rock permeability with the change of effective stress is presented, and the relationships among the permeability, confining pressure and pore pressure are proposed. There are some differences between the dynamic value of permeability-effective-stress coefficient observed herein and the one obtained by the classical theory. Combining with the numerical model and the dynamic permeability, a coupling method for calculating failure pressure is developed. Comparison of field data and calculated values obtained by various methods shows that accurate values can be obtained by the coupling method. The coupling method can be widely applied to the calculation of failure pressure of reservoirs and complex wells to achieve effective fracturing operation.

Transcriptome Analysis of Monozygotic Twin Brothers with Childhood Primary Myelofibrosis

Primary myelofibrosis(PMF) is a chronic myeloproliferative disorder in human bone marrow. Over 50% of patients with myelofibrosis have mutations in JAK2, MPL, or CALR. However, these mutations are rarely detected in children, suggesting a difference in the pathogenesis of childhood PMF. In this study, we investigated the response to drug treatment of a monozygotic twin pair with typical childhood PMF. The twin exhibited different clinical outcomes despite followingthe same treatment regimen. The transcriptomic profiles of patient samples after drug treatment(E2and Y2) were significantly different between the twin pair, which is consistent with the observation that the drug treatment was effective only in the younger brother, despite the twin being genetically identical. Bioinformatics analysis of the drug-responsive genes showed that the JAK-STAT pathway was activated in the cured younger brother, which is opposite to the pathway inhibition observed in adult PMF cases following treatment. Moreover, apoptosis and cell cycle processes were both significantly influenced by drug treatment in the sample of younger brother(Y2), implying their potential association with the pathogenesis of childhood PMF. Gene mutations in JAK2,MPL, or CALR were not observed; however, mutations in genes including SRSF2 and SF3B1 occurred in this twin pair with childhood PMF. Gene fusion events were extensively screened in the twin pair samples and the occurrence of IGLV2-14-IGLL5 gene fusion was confirmed. The current study reported at transcriptomic level the different responses of monozygotic twin brothers with childhood PMF to the same androgen/prednisone treatment regimen providing new insights into the potential pathogenesis of childhood PMF for further research and clinical applications.