Objective To evaluate the clinical effects of combined therapy of Fuyuan Huoxue decoction and transcatheter hepatic arterial chemoembolization in the treatment of primary hepatic carcinoma. Methods 80 patients with primary hepatic carcinoma were randomly divided into a control group, treated by transcatheter hepatic arterial chemoembolization, and a treatment group, additionally treated by Fuyuan Huoxue decoction on the basis of the control group. By observing the change of gross tumor volume、tumor markers、clinical symptoms、Karnofsky Performance Status(KPS) score、quality of life and so on,compare the clinical effects and quality of life between the two groups. Results The effective rate of solid tumor was 47.50%and 35%in the treatment and the control group respectively, with no significant difference(χ2=-1.229, P>0.05);The total effect rate was 87.50%and 32.50%in the treatment and the control group respectively, with significant difference(χ2=-5.633, P<0.05);The rate of patients merged with portal vein tumor thrombus whose cancer embolus narrowed more than 1/2 after the treatment was 78.95%and 33.33%in the treatment and the control group respectively, with significant difference(χ2=7.836, P<0.05);The rate of alpha fetoprotein(AFP) decreasing or turning negative was 78.95%and 37.83%after the treatment in the treatment and the control group respectively, with significant difference(χ2=-3.857, P<0.05);Both groups have improvement in Karnofsky Performance Status(KPS) score after the treatment, the ratios was 80% and 72.50% in the treatment and the control group respectively, with no significant difference(χ2=-1.203, P>0.05);The accumulated scores change of quality of life(QOL) has asignificant difference(χ2=-3.025, P<0.05) between the two groups after the treatment. Conclusion The combined therapy of Fuyuan Huoxue decoction and transcatheter hepatic arterial chemoembolization can alleviate the clinical symptoms, improve treatment effects and quality of life of patients with primary hepatic carcinoma.

OBJECTIVETo investigate the intra-vaginal ejaculation latency time (IELT) of varicocele patients, the influence of spermatic vein ligation on IELT, and the relationship of Visual Analogue Score (VAS) with IELT.

METHODSWe selected 112 males who had regular sexual life after spermatic vein ligation and conducted follow-up visits for 6 months. According to preoperative IELT, we divided the patients into an IELT < or = 2 min group and an IELT > 2 min group, and compared their IELT, VAS and Chinese Index of Sexual Function for Premature Ejaculation-5 (CIPE-5) scores before and 6 months after operation.

RESULTSFollow-up was accomplished in 81 of the patients, 18 in the IELT < or = 2 min group and 63 in the IELT >2 min group. Compared with the baseline, IELT was significantly prolonged postoperatively in both the IELT < or = 2 min group ([1.26 +/- 0.37] vs [4.53 +/- 1.69] min, P < 0.01) and the IELT >2 min group ([5.14 +/- 2.03] vs [7.69 +/- 4.51] min, P < 0.05); the postoperative CIPE-5 scores were remarkably improved in the former (11.27 +/- 3.52 vs 15.64 +/- 2.37, P < 0.05) but insignificantly in the latter group (20.42 +/- 4.65 vs 21.83 +/- 5.49, P > 0.05); the postoperative grades of the CIPE-5 scores showed significant differences in both groups (chi2 = 6.353, P = 0.042 and chi2 = 3.910, P = 0.048); the postoperative VAS was markedly increased (3.18 +/- 0.92 vs 1.56 +/- 0.83 and 3.24 +/- 0.95 vs 1.74 +/- 0.79, P < 0.05), with significant differences in the grades of VAS in both groups (chi2 = 4.433, P = 0.035 and chi2 = 10.088, P = 0.001). The variation of VAS was negatively correlated with that of IELT in both groups (r = -0.572, P < 0.01 and r = -0.465, P < 0.05).

CONCLUSIONVaricocele may be one of the causes of premature ejaculation, and some of the varicocele patients with IELT < or = 2 min may benefit from spermatic vein ligation. Improved VAS is negatively correlated with prolonged IELT. The relationship between varicocele and premature ejaculation deserves further studies.

Adult ; Ejaculation ; physiology ; Follow-Up Studies ; Humans ; Ligation ; Male ; Retrospective Studies ; Varicocele ; surgery ; Young Adult

BACKGROUNDRecent research suggested that obstructive sleep apnea syndrome (OSAS) might be independently associated with hypoadiponectinemia, which was linked to some complications of OSAS, such as hypertension, diabetes, etc. This study was conducted to investigate the effect of continuous positive airway pressure (CPAP) treatment on changes of both serum adiponectin levels and mean arterial pressure and their possible links in male OSAS patients.

METHODSTwenty-three adult male patients with moderate-to-severe OSAS but without obesity, coronary heart disease and diabetes were recruited. Their blood samples were collected and morning mean arterial pressure (MAP) was measured before CPAP treatment and on day 3, 7, 14 of CPAP treatment respectively. The serum adiponectin concentration was tested with radioimmunoassay.

RESULTSCompared with the serum adiponectin level before CPAP treatment, no significant change was found in OSAS patients on day 3 and day 7 of CPAP treatment (P > 0.05). It was not until day 14 of CPAP treatment did a significant elevation in serum adiponectin level occur (P < 0.01). Meanwhile, the MAP showed no statistically significant difference among its levels before CPAP, on day 3 and day 7 of CPAP treatment (P > 0.05). However, on day 14 of CPAP treatment, a significantly lower MAP than that obtained before treatment was observed (P < 0.05).

CONCLUSIONSCPAP treatment can gradually reverse hypoadiponectinemia and reduce MAP in OSAS patients. Hypoadiponectinemia might be involved in the pathogenesis of OSAS-mediated hypertension.

Adiponectin ; blood ; Adult ; Aged ; Blood Pressure ; Continuous Positive Airway Pressure ; Humans ; Male ; Middle Aged ; Sleep Apnea, Obstructive ; blood ; complications ; physiopathology ; therapy

AIM:To investigate the function of microRNA-125a-5p (miR-125a-5p) on epithelial-mesenchy-mal transition ( EMT) of breast cancer cells via GSK-3β/Snail signaling pathway. METHODS:The expression of miR-125a-5p in normal breast epithelial cells and breast cancer cells, as well as the transfection efficiency of miR-125a-5p plas-mid in MDA-MB-231 cells was detected by RT-qPCR. The chemotaxis ability and invasion ability were detected by chemo-taxis assay and Transwell invasion assay. The changes of EMT-related markers, the protein level of phosphorylated glycogen synthase kinase-3β (p-GSK-3β) and the nuclear translocation of Snail were determined by Western blot. RESULTS:The expression of miR-125a-5p in the breast cancer cells was significantly lower than that in the normal breast epithelial cells. The expression of miR-125a-5p was significantly higher in MDA-MB-231/miR-125a-5p cells than that in MDA-MB-231/NC cells. The ability of epithelial growth factor (EGF) at 10 μg/L to induce chemotaxis of MDA-MB-231 cells was the stron-gest. Compared with MDA-MB-231/NC group, stimulation of EGF decreased the invasion ability of MDA-MB-231/miR-125a-5p cells, and resulted in the increase in E-cadherin expression, while significantly decreased the protein levels of vi-mentin and p-GSK-3β. Meanwhile, the nuclear localization of Snail was significantly inhibited. The invasion capacity of MDA-MB-231/miR-125a-5p+GAB2 cells was significantly enhanced compared with MDA-MB-231/miR-125a-5p +Con cells, the expression of E-cadherin was decreased, and the protein levels of vimentin and p-GSK-3β were significantly in-creased, while the nuclear localization of Snail was promoted. CONCLUSION:miR-125a-5p suppresses EMT via GSK-3β/Snail signaling pathway, thus inhibiting the invasion ability of breast cancer cells.

Studies have confirmed that microRNA (miRNAs) is involved in the development and progression of tumors by targeting multiple genes. However, the molecular mechanism of miR-654-5p in in- hibiting the invasion and metastasis of breast cancer cells through the targeted regulation of host cell factor 1 (HCFCl) is still unclear. The analysis of bioinformatics datasets found that miR-654-5p was downregu-lated in breast cancer tissues and was associated with poor prognosis (P = 0. 013). Quantitative real-time PCR (Quantitative real-time PCR, qRT-PCR) showed that the expression of miR-654-5p in MDA-MB-231 cells was decreased (P<0. 05), and the expression of miR-654-5p was significantly increased after transfection of the overexpressed plasmid (P<0. 05) as compared with the control group. The 5-Ethynyl-2'-deoxyuridine (EdU) proliferation experiment and Transwell assay showed that overexpression of miR-654-5p inhibited the proliferation, migration and invasion of MDA-MB-231 cells (P<0. 05). Hub gene HCFCl of miR-654-5p was screened and constructed by Cytoscape software, and it was found that miR-654-5p was negatively correlated with the expression of HCFCl. The expression of HCFCl was increased in breast cancer tissues and closely correlated with lymph node metastasis, and patients with high expression of HCFCl had poor prognosis (P = 0. 0039). Dual-luciferase assay confirmed that miR-654-5p could bind to the 3'-UTR of HCFClmKNA (P<0. 05). Western blot results showed that compared with human normal breast epithelial cells MCF-10A, the expression of HCFCl was increased in MDA-MB-231 cells (P<0. 05), and the expression of HCFCl was significantly down-regulated after overexpression of miR-654-5p (P<0. 05). Transwell experiment results showed that the migration and invasion ability of MDA-MB-231 cells after overexpression of miR-654-5p was significantly decreased compared with the control group. Co-transfection of HCFCl can partially reverse the inhibitory effect of miR-654-5p on the migration and invasion ability of breast cancer cells (P<0. 05). In conclusion, miR-654-5p can inhibit the proliferation, invasion and metastasis of breast cancer cells by regulating the expression of HCFCl.

This study was purposed to investigate the effects of platelet-derived membrane microparticles (PMP) on the proliferation and apoptosis of human umbilical vein endothelial cells (HUVEC). Different concentrations of thrombin were adopted to activate the platelets so as to release PMPs. Flow cytometry (FCM) was adopted to evaluate the efficiencies of different concentrations of thrombin to release PMPs. By using the HUVEC cultivated in vitro as vector, the effects of PMPs on the proliferation and apoptosis of HUVEC were investigated by MTT and FCM. The results showed that the efficiencies releasing PMPs from platelets activated by 2.0, 1.5, 1.0, 0.5 U/ml thrombin were 28.7, 47.7, 50.1 and 43.9% respectively; PMPs induced proliferation of HUVEC in a dose dependent manner. At the concentration of 40 microg/ml PMPs, the proliferation rate of HUVEC was 1.8 +/- 0.3 times as much as blank control, the proliferation rate in group of vascular endothelial growth factor was 1.9 +/- 0.5 times of as much as blank control, there was no statistic difference (p > 0.05). The PMPs inhibited HUVEC apoptosis. Compared with the apoptosis rate of control (9.4 +/- 0.5)%, apoptosis rate in PMP group (40 microg/ml) was (3.9 +/- 0.4)% (p < 0.05). The addition of VEGF (10 microl/ml) did not successfully prevented apoptosis of HUVEC with apoptosis rate of (8.0 +/- 0.8)%. It is concluded that platelets activated by 1 U/ml thrombin gets the best efficiency of PMP release, which stimulates proliferation of HUVEC and inhibits its apoptosis.
Apoptosis ; drug effects ; Blood Platelets ; physiology ; Cell Proliferation ; drug effects ; Cell-Derived Microparticles ; physiology ; Cells, Cultured ; Endothelial Cells ; cytology ; Humans ; Particle Size ; Platelet Membrane Glycoproteins ; physiology ; Thrombin ; pharmacology ; Umbilical Veins ; cytology

OBJECTIVETo study the effect of tetrandrine (Tet) in combination with droloxifen (DRL) on the expression of nuclear factor kappa B (NF-kappaB) in K562 and K562/A02 cell lines and its reversal mechanism.

METHODSThe activation of NF-kappaB in K562 and K562/A02 cell lines and the effect of Tet or DRL alone or in combination on NF-kappaB protein expression were determined with immunocytochemistry and Western blotting respectively.

RESULTS(1) K562/A02 cells displayed higher level of NF-kappaB protein expression than K562 cells. (2) The application of Tet or DRL alone or in combination had no effect on NF-kappaB expression in K562 cells at 6 h and 12 h (P > 0.05). (3) Tet and DRL alone or in combination could significantly down-regulate NF-kappaB protein expression in nuclei of K562/A02 cells. The effect was more significant in combination than either alone. This effect was more significant at 12 h than at 6 h.

CONCLUSIONS(1) Activation of NF-kappaB may be involved in the mechanism of MDR of K562/A02 cell line. (2)Inhibition of NF-kappaB activation may be involved in the reversal of multidrug resistance in K562/A02 cells by Tet and DRL.

Benzylisoquinolines ; pharmacology ; Drug Resistance, Multiple ; Humans ; K562 Cells ; NF-kappa B ; metabolism ; Tamoxifen ; analogs & derivatives ; pharmacology

This study was aimed to investigate the effect of platelet-derived microparticles (PMP) on stimulating the proliferation of granulocyte-macrophage progenitors (CFU-GM) from umbilical cord blood. Different concentrations of thrombin were adopted to activate the platelets for releasing PMP. Flow cytometry was adopted to evaluate the efficiencies of different concentrations of thrombin to produce PMP. Umbilical cord blood mononuclear cells (MNC) were obtained from healthy donors and the MNC were isolated by Ficoll density gradient centrifugation. MNC were cultured in 2.7% methylcellulose containing different concentration of PMP and colonies were counted under an inverted microscope after 7 days. The result showed that the release rate of PMP activated by 2.0, 1.5, 1.0 and 0.5 U/ml thrombin were 28.7%, 47.7%, 50.1% and 43.9% respectively. The PMP enhanced colony formation in dose-dependent manner. The number of colonies per 2 x 10(5) MNCs in groups of PMP at different concentrations (10, 50 and 100 microg/ml) were 119.8 +/- 32.2,142.8 +/- 45.2 and 180.8 +/- 85.1 respectively. The number of colonies in the groups of PMP at 100 microg/ml and 50 microg/ml were statistically significant when compared with control group (103.0 +/- 24.8) (P < 0.05). The number of colonies per 2 x 10(5) MNC in the group of PMP (10 microg/ml) was 119.8 +/- 32.2 which was higher than that in control group, but there was no statistical significance between two groups. It is concluded that platelet activated with 1.0 U/ml thrombin can get the best release efficiency of PMP and PMP can enhance the proliferation of granulocyte-macrophage progenitor cells of umbilical cord blood.
Blood Platelets ; metabolism ; Cell Proliferation ; drug effects ; Cells, Cultured ; Fetal Blood ; cytology ; Granulocyte Precursor Cells ; drug effects ; Humans ; Macrophages ; drug effects ; Phosphatidylserines ; metabolism ; Platelet Activation ; Platelet Factor 3 ; analysis

To study the effects of S-2-(3-aminopropylamino) ethyl phosphorothioic acid (WR-2721, amifostine) on proliferation inhibition and apoptosis of HL-60 human leukemia cell line, the cell apoptosis rate of HL-60 was determined by annexin V/PI double staining method. Cell proliferation and chemotherapy sensitivity were analyzed with XTT assay, and the changes of cell cycle were observed through flow cytometry. The results showed that WR-2721 could significantly inhibit HL-60 cell proliferation. After treatment (30 min, 37 degrees C) with WR-2721, the sensitivity of HL-60 cells to VP16 was enhanced, and the IC(50) descended from 52.5 micro g/ml to 40.5 microg/ml. After 72 hours treatment of HL-60 cells with WR-2721, the early apoptotic cells (annexin V-FITC positive/PI negative) were increased from (5.5 +/- 1.9)% to (48.5 +/- 8.4)% (P < 0.001), late apoptotic cells (annexin V-FITC positive/PI positive) were increased from (1.2 +/- 0.5)% to (39.0 +/- 4.0)% (P < 0.001), and HL-60 cells were arrested in G(2)-M phase. In conclusion, WR-2721 treatment can enhance HL-60 cell chemotherapy sensitivity to VP16, inhibit proliferation, induce apoptosis and accumulation of cells in G(2)-M phase.
Amifostine ; pharmacology ; Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Proliferation ; drug effects ; Drug Synergism ; Etoposide ; pharmacology ; HL-60 Cells ; Humans

This study was purposed to investigate the effects of magnetic nanoparticle of Fe3O4 (Fe3O4-MNPs) on murine immune system. ICR mice were assigned randomly into four groups which were treated with normal saline, low, middle and high dose of MNP-Fe3O4 respectively. The mice were killed after being exposed by intragastric administration for 2 weeks. The ratios of spleen weight to body weight, lymphocyte transformation rate in spleen suspension and phagocytic index of macrophage in abdominal cavity were detected. The results showed that the ratios of spleen weight to body weight in Fe3O4-MNP groups were not significantly different in comparison with the control (p > 0.05). The lymphocyte transformation rate in spleen suspension in Fe3O4-MNP groups were all higher than that in control group (-0.1775 +/- 0.0246), especially in the middle dose group (0.1833 +/- 0.0593) (p < 0.05), and the phagocytic index of macrophages in abdominal cavity of middle dose group (0.2051 +/- 0.0213) was higher than that of control group and other two Fe3O4-MNP group (low dose 0.1538 +/- 0.0100, high dose 0.1511 +/- 0.0184) (p < 0.05). It is concluded that suitable dose of Fe3O4-MNP can enhance the cellular immune activity and phagocytic function of macrophages of mice.
Animals ; Immunity, Cellular ; Lymphocytes ; drug effects ; Macrophages ; drug effects ; Magnetite Nanoparticles ; administration & dosage ; Mice ; Mice, Inbred ICR ; Phagocytosis