Biomedical subjects

Xiang Li

Publications and source records attributed to Xiang Li.

131 records · Page 8Linked to original sources

PubMed2002

[Comparison of the separation performances between semi-preparative chromatographic column and chromatographic pie].

By comparing the resolution and recoveries of proteins between semi-preparative chromatographic column and chromatographic pie (pie-like column) having the same geometric volume under the same chromatographic conditions, the result from the former was found to have the almost same as that form the latter. However, the back pressure of the chromatographic pie rose slower than that of the chromatographic column with the increase of flow rate. Furthermore, the mass and volume loads for the chromatographic pie were higher than those for the chromatographic column. The results indicated that the chromatographic pie had more advantages than the chromatographic column in their performances, and this lay a foundation of the applications of the chromatographic pie in industry.

Chromatography, High Pressure Liquid↗

PubMed2002

[The diagnosis of ectopic thyroid].

OBJECTIVE: To explore the diagnosis method of ectopic thyroid. METHOD: 11 cases with ectopic thyroid were analyzed. RESULT: 11 cases were diagnosed by 99mTc scan, 7 cases were complicated by hypothyroidism, 3 cases were diagnosed by ultrasonography and autopsy else. CONCLUSION: 99mTc scan is the best method and the biopsy is an accurate method to diagnose ectopic thyroid.

Adolescent↗

PubMedDate not supplied

Construction of prostate-specific expressed recombinant plasmids with high transcriptional activity of prostate-specific membrane antigen (PSMA) promoter/enhancer.

To screen different combinations of prostate-specific membrane antigen (PSMA) promoter/enhancer with the strongest transcriptional activity in prostate-specific cells, we used PSMA regulatory elements to control specific expression of the target gene in gene therapy of prostate adenocarcinoma. PSMA promoter and enhancer DNA sequences were amplified from the LNCaP human prostate cancer cell line by polymerase chain reaction, then recombinant plasmids of the enhanced green fluorescent protein (EGFP: pEGFP-PSMA(Pro), pEGFP-PSMA(E-P), pEGFP-PSMA(E(r)-P), pEGFP-PSMA(E(d)-P), and pEGFP-PSMA(E(t)-P)) were constructed with molecular clonal techniques. At the same time, all experimental cell lines were analyzed for the expression of PSMA with the use of PSMA monoclonal antibody and the ABC immunohistochemical assay kit. After plasmids were transfected via liposome, we observed the expression of the reporter gene (EGFP) under a fluorescent microscope and compared the different levels of EGFP expression with reverse transcriptase polymerase chain reaction and flow cytometry so that we could choose the one with the highest transcriptional activity. Only the LNCaP cell line expressed PSMA positively with immunohistochemical stain. The PSMA promoter/enhancer had transcriptional activity in PSMA(+) cell lines and no activity in PSMA(-) cell lines. PSMA(E-P) achieved the strongest activity in different PSMA promoter/enhancer combinations. We confirmed the specific expression of PSMA in prostate cells again. Similarly, transcriptional activity of the PSMA promoter/enhancer was prostate specific. PSMA(E-P) achieved the strongest transcriptional activity among PSMA promoter/enhancer combinations, which could be used in advanced research for tissue-specific treatment.

Antigens, Surface↗

PubMedDate not supplied

Role of extracellular signal-regulated kinase, p38 kinase, and activator protein-1 in transforming growth factor-beta1-induced alpha smooth muscle actin expression in human fetal lung fibroblasts in vitro.

Myofibroblasts characterized by alpha smooth muscle actin(alpha-SMA) expression play a key role in pulmonary fibrosis. Transforming growth factor-beta1 (TGF-beta1) is likely to be involved in the emergence of myofibroblasts, but the intracellular signal pathways for this process have not been well determined. The aim of the present study was to investigate the role of mitogen-activated protein kinase (MAPK)/activator protein-1 (AP-1) signaling pathways in TGF-beta1-induced alpha-SMA expression in human fetal lung fibroblasts (HLF-02). We found that TGF-beta1 treatment activated p38 kinase and extracellular signal-regulated kinase (Erk) in HLF-02 cells. The induction of alpha-SMA by TGF-beta1 was suppressed by p38 kinase inhibitor (SB203580) and Erk inhibitor (PD98059). AP-1 inhibitor curcumin also inhibited TGF-beta1-induced alpha-SMA expression. In addition, dominant negative mutant c-Jun (TAM67) downregulated TGF-beta1-induced AP-1 transactivation and alpha-SMA expression. In additional, PD98059 but not SB203580 inhibited the AP-1 DNA binding activity induced by TGF-beta1. Based on these findings, we conclude that p38 kinase, Erk, and AP-1 are responsible for the alpha-SMA expression induced by TGF-beta1 in human fetal lung fibroblasts. Erk is involved in inducing alpha-SMA expression via AP-1 activation.

Actins↗

PubMedDate not supplied

The hepoxilin analog, PBT-3, inhibits growth of K-562 CML solid tumours in vivo in nude mice.

PBT-3 is one of a family of stable chemical analogs of the hepoxilins, products derived from arachidonic acid. We previously showed that PBT-3 caused apoptosis in the chronic myelogenous leukemia (CML) cell line K-562 in vitro (Anti-cancer Res 23: 3617-3622, 2003). It was as effective as Gleevec, a novel agent that blocks tyrosine kinase activity during treatment of CML. We describe, herein, the growth inhibiting effects of PBT-3 in nude mice into which K-562 cells were transplanted subcutaneously. Groups of mice were treated with vehicle as control, or PBT-3, or Gleevec. PBT-3 was effective during the 8-day treatment protocol in inhibiting the growth of the tumours in vivo as was Gleevec. Analysis of the tumours demonstrated the presence of apoptosis (DNA laddering and TUNEL assay) in both the PBT-3- and Gleevec-treated groups. These results demonstrate that PBT-3 is effective in vivo in controlling tumour growth and provides a novel platform for the therapeutic control of cancer.

8,11,14-Eicosatrienoic Acid↗