To elucidate the effect of angiotensin II (AngII) on the expression of tissue factor (TF) by monocytes and its mechanisms.

To design and make trial of a new therapy for Gaucher disease.

To investigate the molecular mechanisms of saponins from the rhizome of Anemarrhena asphodeloides Bunge.

To obtain a serial differentially expressed cDNA fragments from human osteoblast-like osteosarcoma MG-63 cells induced with 17beta-estradiol and to find some estrogen-responsive genes.

To examine the effects of sodium valproate(VPA) treatment and withdrawal on the expression of GABA transporter-3 (GAT-3) and GABA transaminase (GABA-T) mRNA in C6 glioma cells, and to explore the role of GAT-3 and GABA-T in the rebound mechanism of VPA withdrawal.

To explore the effects of peroxisome proliferator-activated receptor-gamma (PPAR-gamma) on the growth of human lung cancer cell lines and its possible mechanism.

To investigate the effects of glycyrrhizin on genes expression during the process of rat liver fibrosis.

To investigate the effects of cyclosporin A on insulin release and the gene expression profiles of mitochondrial oxidative phosphorylation in NIT-1 cells.

Overexpression of lung resistance-related protein(LRP) is involved in multidrug resistance and poor outcome in acute leukemia. This study was designed to investigate the effect of sodium butyrate (NaB) on LRP expression level and the function of LRP in K562 cells.

To quantitatively evaluate the effects of BMP-2 on the COMP gene expression in both primary human chondrocytes and chondrogenic cell line ATDC55.

To study effect of downregulation of c-myc gene expression with As2O3 on inducing Ec109 cell apoptosis.

To study the influence of adjustment of balance of Th1/Th2 by external cytokines on proliferation of glioma cells.

To study the co-localization of glucocorticoid receptor and 11beta-hydroxysteroid dehydrogenase 1 (11beta-HSD1) and to investigate whether glucocorticoids regulate the reductase activity and expression of 11beta-HSD1.

To investigate the effect of thalidomide on bone marrow cells gene expression in multiple myeloma (MM) patients with suppression subtractive hybridization (SSH) and explore the molecular mechanism of thalidomide therapy for MM.

To explore the effect of T(3) on the expression of transferrin receptor (TfR) and ferritin (Fn) in K562 cells and its possible mechanism.

To investigate the effect of arsenic trioxide (As(2)O(3)) on vascular endothelial growth factor (VEGF) expression in different courses of chronic myeloid leukemia (CML), VEGF level was measured with ELISA in the cultural supernatants of bone marrow mononuclear cells from CML patients. The results showed that supernatants of cultured bone marrow cells from 35 CML patients (20 chronic, 8 accelerated and 7 blast crisis phases) contained significantly higher VEGF levels (649.16 +/- 382.20 pg/ml, 560.27 +/- 409.14 pg/ml and 587.18 +/- 415.28 pg/ml, respectively) than that in 15 normal control samples (152.16 +/- 150.09 pg/ml; P < 0.01), but no significant differences were found in VEGF levels among different phases of CML. The bone marrow cells treated with As(2)O(3) (5 x 10(-6)mol/L) for 72 hours resulted in significant reduction of VEGF levels (down to 396.66 +/- 257.47 pg/ml, 363.42 +/- 239.85 pg/ml and 407.47 +/- 219.38 pg/ml, respectively) (P < 0.05). In conclusion, abnormal high expression of VEGF plays a role in the pathogenetic course of CML and it is probably an additional anticancer mechanism for As(2)O(3) to inhibit VEGF expression of leukemic cells.

This study was designed to explore the influence of STI571, a tyrosine kinase inhibitor, on the expression of c-kit in the bone marrow cells from patients with acute non-lymphocytic leukemia (ANLL). The cells were exposed to various concentration of STI571 for 72 hours, the expression of c-kit mRNA and CD117 was assayed by RT-PCR and flow cytometry, respectively. The results showed that STI571 treatment induced concentration-dependent decrease of c-kit and CD117 expression, which was significant lower than that in group before treatment and untreated control groups (P < 0.05) and 0.1 micro mol/L STI571 group was significantly higher than that in 10 micro mol/L group (P < 0.05). It is concluded that STI571 has an obvious effect on the restraint of c-kit in ANLL cells.

To investigate the correlation between matrix metalloproteinase 9 (MMP-9) expression and tumor invasion and metastasis as well, and to explore the potential application of controlled expression of target gene in tumor gene therapy.

To study the expression levels of ERCC2, UDG, and PCNA in cisplatin-treated A549 cell line.