PubMed Health⌕ Search

Biomedical subjects

L Feng

Publications and source records attributed to L Feng.

267 records · Page 15Linked to original sources
PubMed1986

[O6-methyldeoxyguanosine in DNA of the adjacent epithelium in human esophageal cancer in Linxian County].

Radioimmunoassay of monoclonal antibodies against O6-methyldeoxyguanosine (O6-MedG) was used to detect the presence of these DNA adducts in the human esophageal epithelium. The analysis comprised 48 adjacent epithelial specimens of the esophageal and cardiac cancer resected in Linxian County and 30 specimens of the fetal esophageal epithelium and 4 of the normal esophageal epithelium from autopsy as collected from the hospital in Beijing. The results show that O6-MedG was detected in all the specimens from the esophageal and cardiac cancer patients. In 7 samples in the adjacent epithelium of esophageal cancer, the level of O6-MedG ranged from 0.5 to 1.0 pmol/mgDNA. 19 showed higher levels up to 37.4 pmol/mgDNA with a mean of 4.72 +/- 6.08 pmol/mgDNA. 5 samples of gastric mucosa showed the level of O6-MedG ranging 0.3-1.0 pmol/mgDNA and the remaining 6 showed a higher level of 1.2-13.4 pmol/mgDNA. The mean was 3.31 +/- 3.97. In all the 11 patients, O6-MedG was detected in the para-cancerous gastric mucosa of the cardiac cancer. 4 normal autopsied esophageal epithelial samples were too low for detection. Samples from the fetal esophageal epithelium showed lower level of O6-MedG, the mean was 0.4 +/- 0.57 pmol/mgDNA. The results mentioned above give us the new evidence that the effect of N-nitrosamines is most likely a causative factor in the carcinogenesis of human esophageal cancer.

Cardia↗
PubMedDate not supplied

Expression and characterization of the recombinant juvenile hormone epoxide hydrolase (JHEH) from Manduca sexta.

The cDNA of the microsomal Juvenile Hormone Epoxide Hydrolase (JHEH) from Manduca sexta was expressed in vitro in the baculovirus system. In insect cell culture, the recombinant enzyme (Ms-JHEH) was produced at a high level (100 fold over background EH catalytic activity). As expected, Ms-JHEH was localized in the microsomal fraction with a molecular mass of approximately 50 kDa. Ms-JHEH showed a substrate and inhibitor spectrum similar to the wild type JHEH isolated from eggs of M. sexta. Its enzymatic activity was the highest for Juvenile Hormone III. Ms-JHEH hydrolyzed several trans-epoxides faster than cis-epoxides. A putative hydroxyl-acyl enzyme intermediate was isolated suggesting a catalytic mechanism of Ms-JHEH similar to the mammalian EHs.

Animals↗
PubMedDate not supplied

Toxicity of organic chemicals to fathead minnow: a united quantitative structure-activity relationship model and its application.

A general and practical relation has been established between structure and activity of organic chemicals based on target theory. This relation was tested by examining the correlations between the acute toxicity and the physicochemical properties for fathead minnow, which showed that this relation can explain the observed toxicity data and phenomena successfully. The equations are then used to estimated the acute toxicity data of organic chemicals, and the predicted values are close to observed values.

Animals↗
PubMedDate not supplied

Signaling mechanisms mediating BDNF modulation of synaptic plasticity in the hippocampus.

Although recent studies indicate that brain-derived neurotrophic factor (BDNF) plays an important role in hippocampal synaptic plasticity, the underlying signaling mechanisms remain largely unknown. Here, we have characterized the signaling events that mediate the BDNF modulation of high-frequency synaptic transmission. Mitogen-associated protein kinase (MAPK), phosphotidylinositol-3 kinase (PI3K), and phospholipase C-gamma (PLC-gamma) are the three signaling pathways known to mediate neurotrophin signaling in other systems. In neonatal hippocampal slices, application of BDNF rapidly activated MAPK and PI3K but not PLC-gamma. BDNF greatly attenuated synaptic fatigue at CA1 synapses induced by a train of high-frequency, tetanic stimulation (HFS). Inhibition of the MAPK and PI3K, but not PLC-gamma, prevented the BDNF modulation of high-frequency synaptic transmission. Neurotrophin-3 (NT-3), a close relative of BDNF, did not activate MAPK or PI3K and had no effect on synaptic fatigue in the neonatal hippocampus. Neither forskolin, which activated MAPK but not PI3 kinase, nor ciliary neurotrophic factor (CNTF), which activated PI3K but not MAPK, affected HFS-induced synaptic fatigue. Treatment of the slices with forskolin together with CNTF still had no effect on synaptic fatigue. Thus, although the activation of MAPK and PI3K is required, the two together are not sufficient to mediate the BDNF effect. Inhibition of new protein synthesis by anisomycin or cycloheximide did not prevent the BDNF effect. These data suggest that BDNF modulation of high-frequency transmission is independent of protein synthesis but requires MAPK and PI3K and yet another signaling pathway to act together in the hippocampus.

Animals↗