Objective: To investigate the associations between b 1 -adrenergic receptor (ADRB1) and cytochrome P450 2D6 (CYP2D6) gene polymorphisms and b-blocker treatment outcomes in patients with hypertension. Methods: Chinese patients with essential hypertension were treated with the b-blocker metoprolol and followed up for 12 weeks. xTAG Õ liquid-chip technology was used for CYP2D6 100 C > T and ADRB1 1165G > C genotyping. Associations between gene polymorphisms and antihypertensive therapy outcomes were assessed by generalized linear model fitting. A decrease of ! 10 mmHg in systolic blood pressure indicated an effective treatment outcome. Results: A total of 93 patients were included in the study. Mutant allele frequencies of 61.29% and 58.60% were obtained for ADRB1 and CYP2D6, respectively. There was no significant interaction between the effects of ADRB1 and CYP2D6 gene polymorphisms on treatment outcome. Patients homozygous for the mutant ADRB1 genotype (CC) had better treatment outcomes than those heterozygous for the mutation (GC). Interestingly, b-blocker treatment duration was an independent factor associated with treatment outcome. Conclusions: The ADRB1 1165G > C gene polymorphism and b-blocker treatment duration are independent factors associated with b-blocker treatment outcome. These findings suggest that the selection of antihypertensive therapy should take into consideration the patient's genotype.

The results demonstrate that Gly/Gly polymorphism in Arg389Gly ADRB1 was an independent risk factor together with high fasting plasma glucose, smoking and high triglyceride; moreover, the patients who carried the Gly389Gly genotype had a significantly improved metoprolol antihypertensive effect than those with ADRB1.

MicroRNAs can regulate the transcription of protein-coding genes associated with the development and progression of cancer. In this study, we explored the potential diagnostic function of exosome miR-3184-5p in gastric cancer. This exosome was isolated from the blood samples of 150 patients with gastric cancer and 60 healthy participants.The mean particle size and concentration of serum exosome in the patients with gastric cancer were 104.6 nm (93.97-115.84) and 6.21e+009 particles/ml (5.15e+009-7.12e+009), respectively. miR-3184-5p expression was substantially downregulated in the patients with gastric cancer compared with that in the healthy participants.The gastric cancer cell line HGC-27 was cultured and transfected with the mimic and an inhibitor to overexpress and inhibit miR-3184-5p expression. miR-3184-5p strongly suppressed cell proliferation, migration, and invasion but induced cell apoptosis. Luciferase reporter assay revealed that XBP1 was the target of miR-3184-5p. miR-3184-5p substantially downregulated the expression of CD44, cyclin D1, MMP2, p65, p-AKT, and p-STAT3 but upregulated that of GRP78, IRE1, p-JNK, and CHOP. Moreover, miR-3184-5p cleaved caspase-12 and inhibited BCL-2 expression. These results suggested that the downregulation of miR-3184-5p in patients with gastric cancer might regulate the AKT, STAT3, and IRE1 pathways to promote the vitality of gastric cancer cells.

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