Publications by authors named "Pei-long Lai"

Chronic myelomonocytic leukemia (CMML) treatment remains a pressing clinical challenge. We conducted a retrospective analysis on 52 CMML cases, exploring the effectiveness of combining venetoclax (Vene) with hypomethylating agents (HMAs). The study's findings show promise: the HMAs plus Vene group (n = 13, 53.

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Objective: To establish the in vivo traceable acute myeloid leukemia mice model with Luciferase-Expressing KG1a Cells.

Methods: KG1a cells with stable luciferase gene expression (called as KG1a-Luc cells) were constructed by lentivirus transfection, then sifted out by puromycin. Eighteen male NOD-SCID-IL2rgmice aged 8 to 12 weeks were randomly and equally divided into two groups: the control group and the KG1a-Luc group.

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Objective: To investigate the expression and significance of B and T lymphocyte weakening factor (BTLA) in patients with chronic myelomonocytic leukemia (CMML).

Methods: Real-time PCR was used to detect the expression of BTLA and its ligand HVEM mRNA in 11 patients with chronic myelomonocytic leukemia and 11 normal donors. Flow cytometry was used to detect expression of BTLA and its HVEM on the cell surface of peripheral blood T lymphocytes and γδ T cells.

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Objective: To investigate the effects of exosomes from human umbilical cord mesenchymal stem cells on the development of Treg and TH17 cells.

Methods: Exosomes from the serum-free-culture supernatants of hUC-MSC were harvested by ultracentrifugation. The electron microscopy, nanoparticle tracking analysis and western blot were used to identify the hUC-MSC-exosomes, such as the morphology, the paticle chameter, and the protein content.

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Objective: To explore the clinical efficacy and toxicity of CLAT protocol (cladribine, cytarabine and topotecan) for treating patients with refractory acute myeloid leukemia (R-AML).

Methods: A total of 18 patients with R-AML (median age 37 years, range 18 to 58 years; male n = 16, female n = 2) were treated with CLAT protocol, which consisted of cladribine 5 mg/m(2)/d, i.v.

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Aim: To develop a method for induction of the mouse bone marrow-derived CD8α(+);CD11b(+);jagged2(high);regulatory dendritic cells (DCregs) using mesenchymal stem cells (MSCs) in vitro.

Methods: BALB/c(H-2(d);)mouse bone marrow cells (BMCs) were isolated and induced to CD8α(+);CD11c(+);CD11b(+);DCs (DCs) by 4 cytokines in vitro for 3 d. The DCs were selected by flow cytometry (FCM), and co-cultured with MSCs for 10 d to get DCregs.

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Objective: To analyze the promoter methylation levels of p15, CDH1, DAPK and HICI genes of patients with myelodysplastic syndrome (MDS) and explore the relationship between the level of methylation and clinical features.

Methods: DNA methylation levels of p15, CDH1, DAPK and HICI in peripheral blood (PB) or bone marrow (BM) samples from 52 MDS patients were detected by real-time quantitative PCR. The correlation of the methylation level with clinical features and hematological findings was analyzed.

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