OBJECTIVETo compare the difference in the clinical efficacy on type M prostatitis between the combined therapy of acupuncture and isolated-ginger moxibustion and tamsulosin.

METHODSOne hundred and ten patients of type III prostatitis were randomized into an acupuncture and moxibustion group and a tamsulosin group, 55 cases in each one. In the acupuncture and moxibustion group, acupuncture and isolated-ginger moxibustion were adopted. Two groups of acupoints were selected, named (1) Guanyuan (CV 4), Qugu (CV 2) and Sanyinjiao (SP 6); (2) Yaoyangguan (GV 3), Pangguangshu (BL 28) and Zhibian (BL 54). The two groups of points were used by acupuncture alternatively and only one group was selected a day. Isolated-ginger moxibustion was applied to Guanyuan (CV 4) and Zhibian (BL 54), once a day, 10 treatments made one session, and totally 3 sessions were required. In the tamsulosin group, tamsulosin was prescribed for oral administration, 0.2 mg, twice a day for 1 month. The National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI) score and expressed prostatic secretion (EPS) score were observed in the patients of the two groups.

RESULTSNIH-CPSI and EPS scores after treatment were all reduced apparently as compared with those before treatment in the two groups (all P < 0.05). The improvements in the acupuncture and moxibustion group were more obvious than those in the tamsulosin group (all P < 0.05). In 3 months follow-up, NIH-CPSI score in the acupuncture and moxibustion group was reduced apparently as compared with the tamsulosin group (P < 0.05). The curative rate and total effective, rate were 20.0% (11/55) and 85.5% (47/55) in the acupuncture and moxibustion group, and were 3.6% (2/55) and 61.8% (34/55) in the tamsulosin group respectively (both P < 0.05).

CONCLUSIONThe combined therapy of acupuncture and isolated-ginger moxibustion achieves the good effect of relieving the symptoms of type III prostatitis and recovery of EPS, better than those treated with tamsulosin. This combined therapy spresents the better long-term efficacy.

Acupuncture Points ; Acupuncture Therapy ; Adult ; Ginger ; chemistry ; Humans ; Male ; Middle Aged ; Moxibustion ; Prostatitis ; therapy ; Young Adult

Objective To explore the relationship between levels of serum 25-(OH) D3 and changes in Th1/Th2 cell balance in infants with recurrent wheezing.Methods Sixty cases of infants with recurrent wheezing were involved and 60 cases of healthy children were selected as controls.Enzyme linked immunosorbent assay (ELISA) was used to detect the levels of serum 25-(OH) D3 and double-antibody sandwich (ABC-ELISA) was used to detect the serum levels of interferon-γ(IFN-γ),interleukin (IL)-4,IL-13,and then the relationship between the levels of serum 25-(OH) D3 and changes in Th1/Th2 balance in infants with recurrent wheezing were explored.Results Serum 25-(OH) D3 levels decreased significantly in the infants with recurrent wheezing group compared with those of the healthy control group [(18.24 ± 5.64) μg/L vs (37.85 ± 7.78) μg/L] (t =15.810,P =0.000).Serum IFN-γ levels decreased significantly in the infants with recurrent wheezing group compared with those of the healthy control group [(11.20 ± 2.08) ng/L vs (20.68 ± 3.87) ng/L] (t =16.700,P =0.000).In contrast,serum IL-4,IL-13 levels increased significantly in the infants with recurrent wheezing group compared with those of the healthy control group[IL-4:(28.61 ±6.44) ng/L vs (22.14±5.29) ng/L;IL-13:(20.02±4.83) ng/L vs (17.72± 4.06) ng/L] (t =6.201,P =0.000 ; t =2.829,P =0.006).Th1/Th2 in the infants with recurrent wheezing group were lower than that those of the healthy control group,and there was statistically significant difference between two groups(0.41 ± 0.12 vs 1.00 ± 0.36) (t =11.796,P =0.000).Serum 25-(OH) D3 levels were negatively correlated with Th1/Th2 in the infants with recurrent wheezing(r =-0.649,P =0.000).There were no correlation between serum 25-(OH) D3 levels and Thl/Th2 in the healthy control group(r =-0.217,P =0.096).Conclusions Low serum 25-(OH) D3 may be the risk factor for recurrent wheezing in infants.Serum 25-(OH) D3 levels were negatively correlated with Th1/Th2 in the infants with recurrent wheezing group,which show that recurrent wheezing in the infants is closely related to allergic reaction.

Objective:To explore the relationship between the relative expression of miRNA-676-3p and the survival of renal cancer patients, and its effect on the proliferation and invasion of renal cancer by targeting and regulating prefoldin 1 (PFDN1).Methods:OncoRank online software was selected to analyze the relationship between the relative expression of miRNA-676-3p and the survival rate of renal cancer patients. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the relative expression of miRNA-676-3p in renal cancer cell lines. Renal carcinoma CAKI1 cells were resuscitated, and the transfected miRNA-NC was used as the control group, and the transfected precursor miRNA-676-3p was used as the overexpression group. The relative expression of miRNA-676-3p was detected by RT-qPCR. The cell absorbance and invasion number of the two groups were measured by CCK-8 and Transwell invasion assays, respectively. The target gene of miRNA-676-3p was predicted and verified by referring to the TargetScan Release 8.0 website and dual-luciferase reporter gene experiment. The expression of PFDN1 gene and Wnt/β-catenin molecular pathway protein in the two groups of cells were determined by RT-qPCR and Western blotting, respectively. Measurement data were expressed as mean ± standard deviation ( ± s), t-test was used for comparison between two groups, and one-way analysis of variance was used for comparison between multiple groups. Results:The survival rate of renal cancer patients with high expression of miRNA-676-3p was significantly higher than that of renal cancer patients with low expression of miRNA-676-3p, the difference was statistically significant ( P<0.01). The relative expression of miRNA-676-3p in renal cancer cell lines was significantly lower than that in normal renal tubular epithelial cells, the difference was statistically significant ( P<0.01), and the relative expression of miRNA-676-3p in CAKI1 cells was the lowest, the difference was statistically significant ( P<0.01). The relative expression levels of miRNA-676-3p in the control and overexpression groups were 1.04±0.59 and 15.90±1.70, respectively, and the overexpression group was significantly higher than the control group, the difference was statistically significant ( P<0.01). After 24, 48, 60, and 72 h of culture, the absorbance of cells in the overexpression group was lower than that in the control group, the difference was statistically significant ( P<0.05). The number of invasion cells in the control group and the overexpression group were (115.90 ± 24.73) and (43.83 ± 21.94) cells, respectively, and the number of cell invasion in the overexpression group was significantly lower than that in the control group, the difference was statistically significant ( P<0.01). PFDN1 was the downstream target gene of miRNA-676-3p ( P<0.01). The relative expression of PFDN1 gene in the overexpression group was significantly lower than that in the control group, the difference was statistically significant ( P<0.01). The expression of Wnt/β-catenin molecular pathway proteins in the overexpression group was lower than that in the control group. Conclusions:Renal cancer patients with high expression of miRNA-676-3p had a higher survival rate. miRNA-676-3p inhibited the proliferation and invasion of renal cancer CAKI1 cells by significantly down-regulating the expression of PFDN1, thereby inhibiting the development of renal cancer.

Objective:The relative expression of lncRNA NPIPA9 in prostate cancer tissues was analyzed, and the relative expression of miR-210-3p and its effect on the growth and migration of prostate cancer cells were detected by overexpressing lncRNA NPIPA9.Methods:The relative expression of lncRNA NPIPA9 in prostate cancer tissues was analyzed by Oncomine database. Real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the relative expression of lncRNA NPIPA9 in prostate cancer cell lines DU-145, PC-3, C4-2B, 22Rv1, LNCaP and normal prostate epithelial cell RWPE-1. Prostate cancer PC-3 cells were cultured in vitro and divided into control group (transfected with control vector 100 nmol/L) and NPIPA9 group (transfected with lncRNA NPIPA9 vector 100 nmol/L). The proliferation activity of PC-3 cells was detected by CCK-8 method. The migration ability of PC-3 cells was detected by Transwell method. Potential target of lncRNA NPIPA9 were predicted using bioinformatics techniques. The dual-luciferase reporter gene assay determined the target binding relationship between lncRNA NPIPA9 and miR-210-3p. The effect of lncRNA NPIPA9 on the relative expression of miR-210-3p in prostate cancer cells was detected by RT-qPCR. The effect of lncRNA NPIPA9 on the expression of nuclear factor kappa-B (NF-κB) pathway proteins in prostate cancer cells was detected by Western blotting. Measurement data were expressed as mean±standard deviation ( ± s), and t-test was used for comparison between two groups, one-way analysis of variance was used for comparison between multiple groups. Results:The expression of lncRNA NPIPA9 in prostate cancer tissue was lower than that in adjacent tissue, the difference was statistically significant ( P<0.01). The relative expression of lncRNA NPIPA9 in prostate cancer cell lines was lower than that in RWPE-1 cells, the difference was statistically significant ( P<0.01), and the relative expression of lncRNA NPIPA9 in prostate cancer PC-3 cells was the lowest, the difference was statistically significant ( P<0.01). Compared with the control group, lncRNA NPIPA9 had an inhibitory effect on the viability of prostate cancer PC-3 cells, the difference was statistically significant ( P<0.05). The migration numbers of PC-3 cells in the control group and NPIPA9 group were 101.70±8.63 and 45.97±8.83, respectively, and lncRNA NPIPA9 had an inhibitory effect on PC-3 cell migration, the difference was statistically significant ( P<0.01). lncRNA NPIPA9 can directly target miR-210-3p, the difference was statistically significant ( P<0.01). The relative expression of miR-210-3p in PC-3 cells in control group and NPIPA9 group were 5.32 ± 0.79 and 1.11 ± 0.56, respectively, and lncRNA NPIPA9 could directly down-regulate the expression of miR-210-3p in PC-3 cells, the difference was statistically significant ( P<0.01). Compared with the control group, lncRNA NPIPA9 can reduce the expression of NF-κB pathway proteins c-Myc, MMP-9, VEGF, p65, p50 in PC-3 cells. Conclusion:The expression of lncRNA NPIPA9 is down-regulated in prostate cancer tissues, and it reduces the proliferation and migration ability of prostate cancer PC-3 cells by targeting and negatively regulating miR-210-3p.

Objective:To explore the mechanism by which miRNA-4469 (miR-4469) regulates the proliferation and invasion of renal cancer cells in vitro.Methods:The survival differences of patients with different expression levels of miR-4469 were analyzed based on the OncomiR database. Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) method was used to detect the expression of miR-4469 in renal cancer cell lines ACHN, OS-RC-2, SK-RC-20, 769-P, A498 and normal renal tubular epithelial cell line HK-2, and the renal cancer cells with the lowest expression level of miR-4469 were divided into miR-4469 group and control group, and were transfected with miR-4469 mimic and negative control sequence, respectively. The CCK-8 assay was used to detect the cell proliferation ability (expressed as absorbance value) in the two groups, and Transwell assay was used to analyze the number of invasive cells in the two groups. TargetScan Release 8.0 software was used to predict the binding site between miR-4469 and protein disulfide isomerase A4 (PDIA4) mRNA, and dual-luciferase reporter gene assay was used to verify the targeting relationship between miR-4469 and PDIA4 mRNA. qRT-PCR method was used to detect the expression of PDIA4 mRNA in cells of each group, and Western blotting method was used to detect the expression levels of PDIA4 protein and PI3K-AKT-m-TOR pathway proteins in cells of each group.Results:Analysis of relevant data from the OncomiR database showed that compared with patients with low miR-4469 expression, the overall survival of renal cancer patients with high miR-4469 expression was better ( P < 0.001). The relative expression of miR-4469 in each renal cancer cell line was lower than that in HK-2 cells (all P < 0.05), and the expression of miR-4469 in 769-P cells was the lowest, which were selected to perform the subsequent experiments. The proliferation ability of 769-P cells in the miR-4469 group was lower than that in the control group ( P < 0.01). The number of 769-P cell invasions in the miR-4469 group were less than that in the control group [(19±3) cells vs. (64±7) cells, t = 5.44, P = 0.002]. Compared with the co-transfection of wild-type PDIA4 and miR-4469 negative sequence group, the relative luciferase activity of cells in the co-transfection of wild-type PDIA4 and miR-4469 mimic sequence group was lower (0.42±0.07 vs. 1.01±0.08, t = 5.74, P = 0.001); there was no statistical difference in cell luciferase activity between the co-transfected mutant PDIA4 and miR-4469 negative sequence group and the co-transfected mutant PDIA4 and miR-4469 mimic sequence group (0.99±0.11 vs. 1.02±0.11, t = 0.19, P = 0.001). The relative expression levels of PDIA4 mRNA in 769-P cells in the miR-4469 group were lower than that in the control group (0.98±0.23 vs. 7.19±2.23, t = 2.77, P = 0.032). Compared with the control group, the expression of PDIA4 protein and PI3K-AKT-m-TOR pathway-related p-PI3K, p-AKT, p-mTOR, and p-SGK1 proteins in 769-P cells in the miR-4469 group were all lower (all P < 0.05). Conclusions:miR-4469 may be related to the survival of renal cancer patients, and its expression is down-regulated in various renal cancer cell lines. miR-4469 may inhibit the proliferation and invasion of renal cancer 769-P cells by regulating the PI3K-AKT-m-TOR pathway through PDIA4.