To study the plasminogen activator inhibitors 1 (PAI-1) and matrix metalloproteinases (MMPs) expression on the cultured rat mesangial cells (MsC) transfected with antisense-TGF-beta1 vector.

To investigate the effects and the mechanism of Chinese herb anisodamine on PAI-1 expression in LPS stimulated endothelial cells (ECs).

To investigate the effect of dexamethasone on cultured trabecular meshwork cell growth and the cell expression of epidermal growth factor (EGF) mRNA in vitro.

To study the carcinogenic activity and potential mechanism of the organic extracts from the Songhua River in vitro.

RNAi is a recently developed method to block the activity of cellular genes by artificially providing sense and anti-sense RNA corresponding to a target gene. By inducing rapid degradation of the corresponding endogenous mRNA and blocking new mRNA synthesis, RNAi leads to post-transcriptional gene silencing. Now this phenomenon has been claimed to exist in C. elegans, Drosophila, buds, fungi and plants and is being used to study the functions of some special genes or the known genes at specific time point. It is extremely useful for those genes or organisms that their mutants are not easily obtained. The Drosophila heart related genes, tinman and wingless, have been shown to play an important role in coordinating the early formation of heart progenitor cells and precursors, yet the late function is still unexplored. In this experiment, we took the advantage of RNAi technique, microinjected tinman and wingless dsRNA into the early embryos in Drosophila respectively and got these two genes' RNAi phenotypes, which were very similar to that of their mutant, showing heart tube defects or no heart precursors formation. tinman dsRNA even caused visceral mesoderm defects and the somatic muscles disruption, yet wingless dsRNA only affected heart precursors and had no effect on visceral mesoderm and somatic muscles, indication that the heart-related genes dsRNA interference worked effectively and exclusively in Drosophila.

In the present study, the effects of 17 beta-estradiol on vascular reactivity of ovariectomized rats and proliferation of cultured rat aortic smooth muscle cells were studied. The vascular reactivity was significantly increased in ovariectomized rats compared with the sham-operated animals. The selective ETA receptor antagonist BQ123 inhibited the increase in [3H]-TdR incorporation in response to ET-1 on vascular smooth muscle cells (VSMCs). 17 beta-estradiol also attenuated the ET-1 effects in a dose-dependent manner. The results of RT-PCR and Western blot show that expression of ETA receptor was decreased after treatment with 17 beta-estradiol. The effect of 17 beta-estradiol was partially inhibited by estrogen receptor antagonist tamoxifen. The above results demonstrate that proliferation of VSMCs stimulated by ET-1 was mainly mediated through ETA receptor. Due to the down-regulation of ETA receptor and mediation of estrogen receptor, 17 beta-estradiol inhibits the ET-1-induced proliferation of VSMCs and decreases the vascular reactivity of ovariectomized rats.

To explore the effects of tumor necrosis factor-alpha (TNF-alpha) monoclonal antibody (MAb) on tissue TNF-alpha and lipopolysaccharide-binding protein (LBP) mRNA expression, and multiple organ dysfunction in rats after thermal injury.

To study the induction of apoptosis by retinoid acid(RA) in Tca83 cell line and the expression of correlative Fas/FasL gene.

To investigate multiple-antibiotic-resistance mechanism in clinical strains of Escherichia coli.

To observe the effect of hydroxyurea (HU) alone and in combination with interferon-alpha (IFN-alpha) on the cell growth and cell death, and the related oncogene expression of chronic myelogenous leukemia (CML) cell line, K562 cells. To further investigate the molecular basis of combination therapy on CML by chemotherapeutants combined with cytokines.

To estimate if any difference exists in mRNA expression levels of KATP (SUR1, SUR2, Kir6.2) in heart tissues between streptozotocin-induced diabetic and normal rats, and to examine if any changes of heart KATP in mRNA level occurred after long-term Glibenclamide administration among the diabetic and control rats.

5th instar silkworms were infected with recombinant baculovirus containing phytase gene or wild type BmNPV at 48 hr after ecdysis, then treated with 100 ppm Juvenile hormone. It showed that the expression level of phytase gene and polyhedrin gene per silkworm was increased by 30% and 40%, respectively. The LT50 was lengthened for more than 4 h, and the average weight of sick silkworm was increased by 10%. The results indicated that the improvement of expression efficiency of phytase gene and polyhedrin gene was mainly caused by longer time of virus replication in silkworm after the treatment of Juvenile hormone.

We have identified the bottleneck steps limiting maturation of penicillin G acylase (PAC) through comparison of the maturation performance for various PAC-expression systems (Pac, Tac, T7, Vgb + T7) with different efficiencies of proteolysis, subunit folding and assembly. The maturation of PAC could be limited by various steps, such as translocation, periplasmic proteolysis, subunit folding and assembly depending on the host/vector systems. In BL21(pPA6) cells, maturation of PAC were limited by proteolysis and folding steps; the efficiency of proteolysis was 57.2%; the subunit folding and assembly capacity was 0.72. In BL21(pKKpacSP) cells, the stability and folding of alpha subunit was bottleneck steps. In T7 and dissolved-oxygen regulation expression systems, PAC proprecursor could be maturated efficiently. Results also indicate that the folding of alpha peptide plays a key role in folding of precursor for PAC in E. coli. Developing proper host/vector systems and fermentation technology with superior abilities on subunit folding and assembly of precursor for PAC could be plausible for enhancing production of PAC. In this study, pac could be expressed (transcribed, translated and maturated) efficiently under the control of T7 promoter.

To investigate the mechanism responsible for acquired cisplatin resistance induced in human ovarian cancer cell lines by different methods.

To clarify if there are any correlations between extraneuronal monoamine transmitters (EMT), DNA repair gene expressions and SarCNU antitumor efficacy.

To define chromosome locus of ATRA-induced gene RA109 and intracellular localization of its encoding protein.

To observe the state of Th1/Th2 cytokine expression in peripheral blood mononuclear cells (PBMCs) from asthmatic patients and the effect of erythromycin (Ery) on it.

To study the growth inhibitory and chemo-sensitizing effects of adenovirus E1A gene on HER2/neu-overexpressing tumor cell lines.

To observe the expression of NF-kappa B activation and the effect of dexamethasone on the NF-kappa B activity in the human airway epithelial cell line 16HBE after TNF-alpha stimulation.

Cloning of differentiation-related genes induced by all-trans retinoic acid(ATRA) from human lung cancer GLC-82 cell line.