Effect of hepatocyte growth factor on mice with hypoxic pulmonary arterial hypertension: a preliminary study. / è‚ç»†èƒžç”Ÿé•¿å› å­å¯¹ä½Žæ°§æ€§è‚ºåŠ¨è„‰é«˜åŽ‹å°é¼ å½±å“çš„åˆæ­¥ç ”ç©¶.

OBJECTIVES: To study the association between hepatocyte growth factor (HGF) and treatment response in mice with hypoxic pulmonary arterial hypertension (HPAH) and the possibility of HGF as a new targeted drug for HPAH. METHODS: After successful modeling, the HPAH model mice were randomly divided into two groups: HPAH group and HGF treatment group (tail vein injection of recombinant mouse HGF 1 mg/kg), with 10 mice in each group. Ten normal mice were used as the control group. After 5 weeks, echocardiography was used to measure tricuspid peak velocity, right ventricular systolic pressure, right ventricular hypertrophy index, and right ventricular/body weight ratio; the Griess method was used to measure the content of nitric oxide in serum; ELISA was used to measure the serum level of endothelin-1; transmission electron microscopy was used to observe changes in the ultrastructure of pulmonary artery. RESULTS: Compared with the HGF treatment and normal control groups, the HPAH group had significantly higher tricuspid peak velocity, right ventricular systolic pressure, right ventricular hypertrophy index, and right ventricular/body weight ratio (P<0.05). The transmission electron microscopy showed that the HPAH group had massive destruction of vascular endothelial cells and disordered arrangement of the elastic membrane of arteriolar intima with rupture and loss. The structure of vascular endothelial cells was almost complete and the structure of arterial intima elastic membrane was almost normal in the HGF treatment group. Compared with the normal control and HGF treatment groups, the HPAH group had significantly higher serum levels of nitric oxide and endothelin-1 (P<0.05). CONCLUSIONS: Increasing serum HGF level can alleviate the impact of HPAH on the cardiovascular system of mice, possibly by repairing endothelial cell injury, improving vascular remodeling, and restoring the normal vasomotor function of pulmonary vessels.

Progress of Clinical Application of SNP-A to MDS--Review / 中国实验血液学杂志

Cytogenetic abnormalities get wide attention for its guidance value for prognosis and therapy in myelodysplastic syndrome (MDS) and related malignancies. Cytogenetic analysis is also the key to clarify the molecular pathogenesis of these kinds of diseases. The traditional karyotyping technique including metaphase cytogenetic (MC) karyotype analysis and immune fluorescence in situ hybridization (FISH) can detect the chromosomal abnormalities to some degree while the positive rate detected by the techniques is low due to the low resolution, dependence on metaphase dividing cells or the limitation of specific sites on the chromosomes, respectively. Although array comparative genomic hybridization (aCGH) makes up for some deficiencies of the techniques above, only copy number variations (CNVs) could be detected by aCGH. Recently, single nucleotide polymorphasim array (SNP-A) are employed to detect chromosomal CNVs and uniparental disomies (UPDs) which are significant for illumination of the pathogenetics and prognosis of MDS. Based on the detection principle and characteristics of SNP-A, this article reviews the clinical application and prospect of the technique in aspect of the detection characteristic of SNP-A, the relationship between cryptic aberrations and MDS related aspects including the pathogenic genes, phenotypes, prognosis, stratification system and self control test.