[Effect of Knocking Out Gene by CRISPR-Cas9-Mediated Gene Editing Technique on Proliferation of Acute Myeloid Leukemia Cells].

Objective: To construct a acute myeloid leukemia (AML) cell line in which gene is stably knocked out by CRISPR-Cas9-mediated gene editing technique, so as to clarify the effect of gene knockout on the proliferation of AML cells, and preliminarily explore the role of gene in the pathogenesis of AML.

Methods: The expression of HOXA5 in bone marrow mononuclear cells (BMMC) of non-tumor hematological patients and newly diagnosed AML patients was detected by quantitative real-time PCR (qRT-PCR) and Western blot, respectively. The AML cell line KO-HOXA5-THP-1 was constructed in which gene was knocked out by CRISPR-Cas9-Mediated gene editing technique, and the knockout of HOXA5 gene was verified by qRT-PCR and Western blot, and the cell proliferation was detected by CCK-8 assay.

Endovascular treatment for massive haemoptysis due to pulmonary pseudoaneurysm: report of 23 cases.

Purpose: To evaluate the safety and effectiveness of endovascular treatment for massive haemoptysis caused by pulmonary pseudoaneurysm (PAP).

Methods: The clinical data, imaging data, and endovascular treatment protocol of 23 patients with massive haemoptysis caused by continuous PAP were retrospectively analysed. The success, complications, postoperative recurrence rate, and influence of the treatment on pulmonary artery pressure were also evaluated.

[Effects of TLR4-PI3K-Rac1 pathway on cytoskeleton rearrangement and phagocytosis of macrophage].

To investigate the effects of Toll-like receptor 4 (TLR4)-phosphatidylinositol 3-kinase (PI3K) -Ras-related C3 botulinum toxin 1 (Rac1) signaling pathway on macrophage cytoskeleton rearrangement and phagocytosis. Mouse macrophage cell line RAW264.7 was divided into blank group, negative control group and TLR4-RNA interference (RNAi) group.

[Effects of PI3Kδ-RhoA pathway on phagocytosis defect of alveolar macrophages in a mouse model of chronic obstructive pulmonary disease].

To investigate effects of Phosphoinositide3-Kinases (PI3Kδ)-Ras homolog gene family member A(RhoA) pathway on phagocytosis deficiency of alveolar macrophages (AMs) in a mouse model of chronic obstructive pulmonary disease (COPD). Twenty mice were exposed to cigarette smoking to establish the COPD model, with 20 mice as the control group. AMs were isolated from lung tissue by discontinuous density gradient centrifugation and then divided into a healthy control group, a COPD group, a healthy IC87114 group and a COPD IC87114 group.

[Mechanisms of cytoskeleton and PI3Kδ-RhoA in fine particulate matter deteriorating phagocytosis defect of alveolar macrophage in mice with chronic obstructive pulmonary disease].

To explore the mechanism of cytoskeleton and PI3Kδ-RhoA in fine particulate matter deteriorating phagocytosis defect of alveolar macrophage (AM) in chronic obstructive pulmonary disease (COPD) mice. Forty mice were randomly divided into four groups: health control group, COPD group, health PM2.5 group, COPD PM2.

[Effects of mTOR-Cdc42 signaling pathway on phagocytosis of alveolar macrophages in chronic obstructive pulmonary disease mice].

To investigate effects of mammalian target of rapamycin (mTOR)- cell division cycle 42 (Cdc42) signaling pathway on phagocytosis of alveolar macrophages (AMs) in chronic obstructive pulmonary disease (COPD) mice. Forty mice were randomly divided into control group and model group. Each group contained 20 mice.