Jiao Binghua

Dihydrochalcones and phenanthrene derivatives from Fissistigma bracteolatum

Three dihydrochalcones derivatives 1-3, flavone 4 and phenanthrene derivative 5 were isolated, together with 9 known compounds, from the air-dried root bark of Fissistigma bracteolatum Chatterjee. Their structures were determined by spectroscopic (NMR, MS) and chemical methodologies.

Detection of Mitochondrial DNA Deletion by a Modified PCR Method in a 60Co Radiation‐exposed Patient

A new PCR based method was developed to detect deleted mitochondrial DNA (mtDNA). Peripheral blood cell DNA was obtained from a victim who was accidently exposed to a 60Co radiation source in 1990. Using the DNA as template, first PCR was performed to generate multiple products including true deletions and artifacts. The full length product was recovered and used as template of secondary PCR. The suspicious deletion product of mtDNA could be confirmed only if it was yielded by first PCR. Using either original primers or their nested primers, the suspicious deletion product was amplified and authenticated as a true deletion product. The template was recovered and determined to be a deletion by sequencing directly. The results show that a new mtDNA deletion, which spans 889 bp from nt 11688 to nt 12576, was detected in the peripheral blood cells of the victim. It indicates that this new PCR‐based method was more efficient at detecting small populations of mtDNA deletion than other routine methods. MtDNA deletion was found in the victim, suggesting the relationship between the deletion and phenotypes of the disease. IUBMB Life, 55: 133‐137, 2003

Search for difference in aminoacylation of mitochondrial DNA-encoded wild-type and mutant human tRNALeu(UUR)

The pathogenetic mechanism of the most extensively investigated A3243G mutated tRNALeu (UUR) gene, which causes the MELAS encephalomyopathy, maternally inherited diabetes, or chronic progressive external ophlthalmoplegia, is still unresolved, despite the numerous investigations on the topic. Previous evidences presented in published work suggested that the mitochondrial DNA harboring A3243G mutation result decreases in the rates of mitochondrial protein synthesis. To search for differences in aminoacylation of mitochondrial DNA‐encoded wild‐type and mutant human tRNALeu (UUR), we have expressed and purified the two kinds of tRNAsLeu (UUR), and have expressed human mitochondrial leucyl‐tRNA synthetase for in vitro assays of aminoacylation of wild‐type and mutant human tRNALeu (UUR). The results indicate human mitochondrial tRNALeu (UUR) gene A3243G point mutant can remarkably reduce its aminoacylation, suggesting it could be one of the mechanisms that the mutation can produce in such clinical phenotypes. IUBMB Life, 55: 139‐144, 2003