The results suggest that 12 days of treatment with Ginkgo biloba did not significantly alter the single-dose pharmacokinetics of voriconazole in either CYP2C19 extensive or poor metabolizers. Therefore, the pharmacokinetic interactions between voriconazole and Ginkgo biloba may have limited clinical significance.
BACKGROUND
The drug resistance rate of clinical
Helicobacter pylori
(
H. pylori
) isolates has increased. However, the mechanism of drug resistance remains unclear. In this study, drug-resistant
H. pylori
strains were isolated from different areas and different populations of Chinese for genomic analysis.
AIM
To investigate drug-resistant genes in
H. pylori
and find the genes for the early diagnosis of clarithromycin resistance.
METHODS
Three drug-resistant
H. pylori
strains were isolated from patients with gastritis in Bama County, China. Minimal inhibitory concentrations of clarithromycin, metronidazole, and levofloxacin were determined and complete genome sequencing was performed with annotation.
Hp1181
and
hp1184
genes were found in these strains and then detected by reverse transcription polymerase chain reaction. The relationships between
hp1181
or
hp1184
and clarithromycin resistance were ascertained with gene mutant and drug-resistant strains. The homology of the strains with
hp26695
was assessed through complete genome detection and identification. Differences in genome sequences, gene quantity, and gene characteristics were detected amongst the three strains. Prediction and analysis of the function of drug-resistant genes indicated that the RNA expression of
hp1181
and
hp1184
increased in the three strains, which was the same in the artificially induced clarithromycin-resistant bacteria. After gene knockout, the drug sensitivity of the strains was assessed.
RESULTS
The strains showing a high degree of homology with
hp26695
,
hp1181
, and
hp1184
genes were found in these strains; the expression of the genes
hp1184
and
hp1181
was associated with clarithromycin resistance.
CONCLUSION
Hp1181
and
hp1184
mutations may be the earliest and most persistent response to clarithromycin resistance, and they may be the potential target genes for the diagnosis, prevention, and treatment of clarithromycin resistance.
Background. Interleukin-2 (IL-2) is proved to play an irreplaceable role in antitumor regulation in numerous experimental and clinical trials. Tumor-associated macrophages (TAMs) are able to release exosomes to promote the development and progression of hepatocellular carcinoma (HCC) as essential component of microenvironment. In this study, our intention is to explore the effects of the exosomes from TAMs with IL-2 treatment on HCC development. TAMs were collected and cultured from HCC tissues. The exosomes from the TAMs treated with IL-2 (ExoIL2-TAM) or not (ExoTAM) were identified and used to treat HCC cells in vivo and in vitro. The proliferation, apoptosis, and metastasis of HCC cells were measured. The changes of miRNAs in exosomes were explored to clarify the possible mechanisms. Both decrease of cell proliferation and metastasis and increase of apoptosis were observed with ExoIL2-TAM treatment compared with ExoTAMin vivo and in vitro. miR-375 was obviously augmented in ExoIL2-TAM and HCC cells treated with ExoIL2-TAM. Taken together, IL-2 may modulate exosomal miRNAs from TAMs to ameliorate hepatocellular carcinoma development. This study provides a new perspective to explain the mechanism by which IL-2 inhibits hepatocellular carcinoma and implies the potential clinical value of exosomal miRNAs released by TAMs.
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