Infant acute myeloid leukemia（IAML）is a clinically rare hematological malignancy.Compared to older children，IAML patients usually have significantly higher-risk biological characteristics，namely a low induction remission rate and a high recurrence risk.Although continuous research has been conducted on its molecular mechanisms and treatment methods，the 5-year survival rate by traditional treatment regimens is only 50%~60%.Therefore，targeted therapies，such as CD33 monoclonal antibodies，and cellular immunotherapy，have become key strategies to overcome treatment barriers.This article reviews the progress on the molecular characteristics of IAML，the efficacy and challenges of traditional chemotherapy optimization schemes and targeted therapy，as well as CAR-T cell immunotherapy.

OBJECTIVE: To explore the influence of gender of chromosomal translocation carriers on the occurrence of embryonic chromosomal aberrations. METHODS: A retrospective study was carried out. Data were collected from 235 couples carrying reciprocal translocations (1163 blastocysts) and 70 couples carrying Robertsonian translocations (351 blastocysts). The preimplantation genetic testing for structural rearrangement (PGT-SR) analysis of 1514 blastocysts were completed through next generation sequencing (NGS). RESULTS: After adjusting the confounding factors such as female age, AMH, ovarian stimulation regimen, and Gn dosage, the results showed that the risk for blastocyst chromosomal abnormalities was 0.41 [OR(95%CI), 1.41(1.06, 1.87), P < 0.05] times higher in female reciprocal translocation carriers and 1.02 [OR(95%CI), 2.02 (1.20, 3.40), P < 0.01] times higher in female Robertsonian translocation carriers compared with male carriers, respectively. Compared with male carriers, the risk of blastocyst chromosomal abnormalities was increased by 0.67 times [OR(95%CI), 1.67 (1.10, 2.56), P < 0.05] in female reciprocal translocation carriers over 30 years old and 1.06 times [OR(95%CI), 2.06 (1.02, 4.15), P = 0.0434, P < 0.05] in female Robertsonian translocation carriers between 25 and 30 years old. CONCLUSION Compared with male carriers, female carriers of reciprocal or Robertsonian translocations have a higher risk for producing embryos with chromosomal abnormalities, and their age may also be a risk factor.
Adult ; Blastocyst ; Chromosome Aberrations ; Female ; Genetic Testing/methods* ; Humans ; Male ; Pregnancy ; Preimplantation Diagnosis/methods* ; Retrospective Studies ; Translocation, Genetic

Objective:to apply Fuzhengkangai AIDS particles combined therapy with effective antiretroviral therapy (HAART) at the beginning of the HIV/AIDS (human immunodeficiency virus/acquired immunodeficiency syndrome) patients,observe its clinical curative effect and improve the related adverse reactions.Methods:a multicenter,randomized,double-blind,placebo-controlled clinical research method,divided into experimental group and the control group (n =57),experimental group to "Fuzhengkangai particles" joint efficient antiretroviral therapy (HAART) antiviral treatment,control group to "Fuzhengkangai particles" placebo (5％ low dose) joint efficient antiretroviral therapy (HAART) antiviral treatment,treatment for 3 months.Two groups of patients with simultaneous liver and kidney function,blood routine,CD4 + T lymphocyte count,the observation of TCM symptoms and signs,survival quality of integral.Results:after 12 weeks of treatment,the control group and experimental group,the experimental group significantly elevated levels of peripheral blood RBC,lower levels of CR,reduce the signs and symptoms (total score,fatigue,stay,and spontaneous perspiration)integral,higher levels of CD4 + T lymphocyte count and survival quality score,the difference had statistical significance (p ＜ 0.05).Conclusion:Fuzhengkangai particles joint efficient antiretroviral therapy (HAART) antiviral treatment,can improve HAART after initial treatment of the patient's clinical symptoms,blood toxicity,the quality of survival,reduce the antiviral treatment of adverse reactions,combination drug alone can significantly increase the CD4 + T lymphocytes,so as to improve clinical curative effect.

Objective To investigate the effects and mechanisms of rosiglitazone on the expressions of nuclear factor-κB and matrix metalloprotease (MMP-9) in peripheral blood monocyte-derived macrophages (MDMs) in patients with coronary heart disease. Method This was a clinical case-control study. Forty-eight actue coronary symdrome (ACS) patients (ACS group), and 20 patients with stable angina (SA) (control group) were collected. They were performed coronary arteriography in the Department of Cardiology of the Second Xiangya Hospital from March to April in 2007. Exclusion criteria included acute infection, trauma or surgery patients within four weeks, cerebral vascular accident, liver and kidney dysfunction, cancer, and so on. The peripheral blood mononuclear cells were isolated and transformed into MDMs with macrophage colony-stimulating factor treatment. The transformed MDMs were randomly assigned into subgrougs and incubated with 0 /μmol/L, 1 μmol/L, 10 μmol/L, 20 μmol/L of rosiglitazone respectively. The expressions of PPAR-γ mRNA, MMP-9 mRNA were determined by RT-PCR and nuclear factor-κB P65 (NF-KB P65) expression by immunohistochemistry. Multiple comparisons were examined for significant differences using analysis of variance (ANOVA). Results The basal expression of PPAR-y mRNA was lower, in contrast, the levels of NF-KB P65 and MMP-9 mRNA were higher in ACS group than control group. PPAR-γ mRNA expression were significantly upregulated in both ACS and control groups with rosiglitazone treatment. PPAR-γ mRNA expression was positive correlation, while the expressions of MMP-9 mRNA were negative correlation with the rosiglitazone concentration in the ACS group. Rosiglitazone inhibited the expression of NF-KB in a concentration-independent manner in ACS and control groups. Conclusions The expression of PPAR-y mRNA is inhibited, while the activity of NF-KB and expression of MMP-9 mRNA are enhanced in MDMs of ACS cases. Rosiglitazone intervention may inhibit NF-KB activity and MMP-9 expression by upregulation of PPAR-y expression in MDMS of patiens with ACS.