To understand whether endotoxin lipopolysaccharide (LPS) is able to induce the expression of macrophage inflammatory protein-1alpha (MIP-1alpha) mRNA and protein in human umbilical vein endothelial cells (HUVECs).

To investigate the effect of Shen-Mai injection (SMI) and aminophylline on diaphragmatic muscle cell apoptosis and the Fas/FasL expression in chronic hypoxic rats.

To explore the effects of arsenic trioxide (As2O3) on tissue factor (TF), plasminogen activator inhibitor-1(PAI-I) and PAI-2 expression in NB4, HL-60 and THP-1 cells.

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.