Objective: A method for the determination of gallic acid in the extract of Quercus salece- na Blume (Fagaceae) and its preparation (Urocalum Capsules) by means of RP-HPLC was established. Method: The hydrolysable tannins contained in the sample is hydrolyzed with hy- drochloric acid, the hydrolysis component-gallic acid is determined by HPLC using RP-C18 column, 0.005mol. L-1 of phosphoric acid-methanol (98: 2) as mobile phase , 270 nm as detec- tion wavelength. Result: The linear range of gallic acid is 0. 3～3. 1?g , r=0. 9999, the average recovery is 100. 4%. Conclusion: It is confirmed that the established method for assay of gallic acid meet the criteria of quantitative analysis of herbal medicine by validation of hydrolysis condition, repeatebility, stability and recovery, The method is simple , good reproducible and precise , and it can also be applied to analysis of other herbal medicine containing hydrolysable tannins.

OBJECTIVETo analyze the loss of heterozygosity (LOH) of chromosome 20 in patients with sporadic colorectal cancer to identify additional loci involved in colorectal tumorigenesis.

METHODSPolymorphic microsatellite markers were analyzed in 83 colorectal cancer patients' tumor and normal DNA by PCR. PCR products were electrophoresed on an 377 DNA sequencer. Genescan 2.1 and Genotype 2.1 software were used in the LOH scanning and analysis. Comparisons between LOH frequency and clinicopathological data were performed by chi(2) test. P < 0.05 was considered statistically significant.

RESULTSThe average LOH frequency in the long arm, short arm and whole chromosome 20 was 21.1%, 26.7% and 22.8%, respectively. Chromosome 20 exhibited relatively high LOH frequency, particularly in the regions of 20p and 20q11.1-q13.1.

CONCLUSIONThere is notable genetic instability on chromosome 20 in sporadic colorectal carcinoma patients; that is, mutation on chromosome 20 is closely associated with sporadic colorectal carcinogenesis. Also, there may be tumor suppressor genes related to sporadic colorectal carcinoma near the region 20q11.1-q13.1.

Adult ; Aged ; Aged, 80 and over ; Chromosomes, Human, Pair 20 ; Colorectal Neoplasms ; genetics ; pathology ; Female ; Humans ; Loss of Heterozygosity ; Male ; Microsatellite Repeats ; Middle Aged

Long noncoding RNAs (lncRNAs) play a critical role in the regulation of atherosclerosis. Here, we investigated the role of the lncRNA growth arrest-specific 5 (lncR-GAS5) in atherogenesis. We found that the enforced expression of lncR-GAS5 contributed to the development of atherosclerosis, which presented as increased plaque size and reduced collagen content. Moreover, impaired autophagy was observed, as shown by a decreased LC3II/LC3I protein ratio and an elevated P62 level in lncR-GAS5-overexpressing human aortic endothelial cells. By contrast, lncR-GAS5 knockdown promoted autophagy. Moreover, serine/arginine-rich splicing factor 10 (SRSF10) knockdown increased the LC3II/LC3I ratio and decreased the P62 level, thus enhancing the formation of autophagic vacuoles, autolysosomes, and autophagosomes. Mechanistically, lncR-GAS5 regulated the downstream splicing factor SRSF10 to impair autophagy in the endothelium, which was reversed by the knockdown of SRSF10. Further results revealed that overexpression of the lncR-GAS5-targeted gene miR-193-5p promoted autophagy and autophagic vacuole accumulation by repressing its direct target gene, SRSF10. Notably, miR-193-5p overexpression decreased plaque size and increased collagen content. Altogether, these findings demonstrate that lncR-GAS5 partially contributes to atherogenesis and plaque instability by impairing endothelial autophagy. In conclusion, lncR-GAS5 overexpression arrested endothelial autophagy through the miR-193-5p/SRSF10 signaling pathway. Thus, miR-193-5p/SRSF10 may serve as a novel treatment target for atherosclerosis.
Humans ; Atherosclerosis/genetics* ; Autophagy/genetics* ; Cell Cycle Proteins/metabolism* ; Endothelial Cells/metabolism* ; Endothelium/metabolism* ; MicroRNAs/metabolism* ; Repressor Proteins/metabolism* ; RNA Splicing Factors ; Serine-Arginine Splicing Factors/genetics* ; RNA, Long Noncoding/metabolism*