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The neural stimulator is a core component of animal robots. While the control effect of animal robots is influenced by various factors, the performance of the neural stimulator plays a decisive role in regulating animal robots. In order to optimize animal robots, embedded neural stimulators had been developed using flexible printed circuit board technology. This innovation not only enabled the stimulator to generate parameter-adjustable biphasic current pulses through control signals, but also optimized its carrying mode, material, and size, overcoming the disadvantages of traditional backpack or head-inserted stimulators, which have poor concealment and are prone to infection. Static, in vitro, and in vivo performance tests of the stimulator demonstrated that it not only had precise pulse waveform output capability, but also was lightweight and small in size. It had excellent in vivo performance in both laboratory and outdoor environments. Our study has high practical significance for the application of animal robots.
Assuntos
Animais , RobóticaRESUMO
Objective:To investigate the effect of resveratrol (Res) on the fat synthesis in the liver cancer HepG2cells, and to elucidate its possible mechanism.Methods:The HepG2cells were cultured in vitro and divided into Res group (treated with 40μmol·L-1 DMSO-diluted Res for 24h) and control group (treated with the same concentration of DMSO for 24h) .The cell supernatant was collected, and the levels of triglyceride (TG) and total cholesterol (TC) in the cells in various groups were measured by ELISA.The mRNA and protein expression levels of lipase synthase acetyl-CoA carboxylase (ACC1) , fatty acid synthetase (FASN) and stearoyl-CoA desaturase (SCD1) in the cells in various groups were detected by qRT-PCR and Western blotting method.The levels of O-linked N-acetylglucosamine (O-GlcNAc) glycosylation in the cells in various groups were detected by Western blotting method.Results:Compared with control group, the levels of TG and TC in the cells in Res group were decreased, but the difference was not statistically significant (t1=1.886, P>0.05;t2=2.457, P>0.05) .Compared with control group, the levels of expressions of ACC1, FASN and SCD1mRNA and proteins in the cells in Res group were significantly decreased (P<0.05or P<0.01) ;the O-GlcNAc glycosylation level in the cells in Res group was significantly decreased (t=2.87, P<0.05) .Conclusion:Res has the effect of inhibiting the fat synthesis in the liver cancer HepG2 cells.Its mechanism may be related to the reduction of cellular O-GlcNAc glycosylation level and the reduction of the expression of FASN.
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Objective To investigate the roles and mechanisms of hepatocyte nuclear factor 4α (HNF4α) in chenodeoxycholic acid (CDCA) induced gastric intestinal metaplasia (IM).Methods After the immortalized gastric mucosal epithelial cells GES-1 were stimulated with CDCA at different concentration,the changes of HNF4α,caudal-related homeobox 2 (CDX2) and trefoil factor family 3 (TFF3) expressions at mRNA and protein levels in GES-1 cells and gastric cancer cell lines (AGS,SGC7901 and BGC823) were detected by real time-polymerase chain reaction (RT-PCR) and Western blotting.After GES-1 were transfected with HNF4α short hairpin RNA (shRNA) or control shRNA,and followed by CDCA stimulation,the expressions of HNF4α,CDX2 and TFF3 at protein level were determined by Western blotting.HNF4α was overexpressed in GES-1 cells and SGC7901 cells,and HNF4α was silenced in BGC823 cell line and AGS by lentiviral vector system.The expressions of HNF4α,CDX2 and TFF3 at mRNA and protein levels were tested by RT-PCR and Western blotting.Luciferase reporter assay was used to analyze the regulation role of HNF4α on CDX2.T test was performed for statistical analysis.Results The expressions of HNF4α in GES-1,SGC7901,BGC823 and AGS cells at mRNA level were 1.00 ± 0.12,263.01±10.23,848.01±18.13 and 3 049.86±91.75,respectively.The mRNAlevels of HNF4α in AGS,BGC823 and SGC7901 cells were all higher than that of GES-1 cells,and the differences were statistically significant (t=33.23,46.72 and 25.62,all P<0.01).The expressions of HNF4α in GES-1,SGC7901,BGC823 and AGS at protein level were consistent with mRNA level.The expressions of CDX2 and TFF3 at protein level of HNF4α shRNA transfected group were lower than those of non-HNF4α shRNA transfected group.In GES-1 cells,the expressions of HNF4α,CDX2 and TFF3 of HNF4α overexpressed group at mRNA level were 16 281.839 ± 1 843.017,6.275 ± 0.137 and 17.310± 1.533,respectively;which were all higher than those of overexpressed control group (1.000 ± 0.048,1.000 ± 0.012 and 1.000±0.108,respectively),and the differences were statistically significant (t =8.83,38.29 and 10.61,all P<0.01).In AGS cells,the expressions of HNF4α,CDX2 and TFF3 of HNF4α silenced group at mRNA level were 0.021 ± 0.001,0.088 ± 0.007 and 0.074 ± 0.002,respectively,which were lower than those of silenced control group (1.000 ± 0.108,1.000 ± 0.131 and 1.000 ± 0.122),and the differences were statistically significant (t=9.09,6.93 and 7.57,all P<0.01).In GES-1 overexpressed cells and AGS silenced cells,the expressions of HNF4α,CDX2,TFF3 at protein level were consistent with mRNA level.In double reporter plasmid containing the CDX2 promoter CDX2 1 (-2 000~-1 bp) and CDX2-2 (-1 510~1 bp),after transfected with HNF4α shRNA,the activities were 0.387 ± 0.013 and 0.533 ± 0.040,respectively,which were lower than those of HNF4α shRNA transfected control group (0.605 ± 0.012 and 0.882 ± 0.019),and the differences were statistically significant (t =21.49 and 13.53,both P<0.01).Conclusion HNF4α may be involved in bile acid induced intestinal metaplasia by upregulating the expression of CDX2.
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Objective To explore the therapeutic effects of the folic acid,vitaminB12on Helicobacter pylori(Hp)-negative patients with chronic atrophic gastritis(CAG).Methods we enrolled 67 patients who were diagnosed as CAG of Hp-negative from the First Affiliated Hospital of Xi′an Medical University.The patients were divided into control group and treatment group. Control group were given routine treatment(pepsin tablets), treatment group were given routine treatment and folic acid,vitaminB12. Then respective compared the folic acid, vitaminB12,clinical symptoms scores,gastroscopic scores and histopathological scores in the two groups before treatment and after treatment of 12 weeks and 24 weeks.Results After treatment of 12 weeks,there were signifi-cant differences in the gastroscopic scores and histopathological scores(activity),folic acid,vitaminB12status (P<0.05);no significant difference existed in clinical symptoms scores,histopathological scores(chronic inflam-mation,atrophic,intestinal metaplasia)between the two groups(P > 0.05). After treatment of 24 weeks,the differences of clinical symptoms scores,gastroscopic scores,histopathological scores(chronic inflammation, activity,atrophic,intestinal metaplasia)and folic acid,vitaminB12status were significant(P < 0.05);no significant difference existed in histopathological scores(intestinal metaplasia)between the two groups(P >0.05). Conclusion Folic acid and vitaminB12can improve the clinical symptoms and histological situation of the Hp-negative patients with CAG,worthy of further popularizing in clinic.
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Objective To quantitatively analyze the mRNA expression level of lymphoid enhance factor 1 (LEF-1) in bone marrow mononuclear cells of patients with acute myeloid leukemia (AML) at intermediate-risk after initial diagnosis and chemotherapy, and to analyze its clinical significance. Methods The real-time fluorescence quantitative polymerase chain reaction (RT-PCR) was used to measure the expression level of LEF-1 gene in AML patients at intermediate-risk after initial diagnosis and chemotherapy, and its relationship with effectiveness and survival were analyzed. Results The LEF-1 mRNA level in preliminarily diagnosed patients with AML was significantly higher than that in control arm [0.00519 (0.00015-0.09207) vs. 0.00101 (0.00009-0.00233)], and the difference was statistically significant (u=134.50, P<0.01). The LEF-1 mRNA level in patients after chemotherapy was significantly declines as compared to that in patients before chemotherapy [0.00107 (0.00008 - 0.00744) vs. 0.00519 (0.00015 - 0.09207)], and the difference was statistically significant (u= 317.00, P< 0.01) and LEF-1 mRNA expression level before chemotherapy in complete remission (CR) patients was significantly higher than that in non-CR patients [(0.01108 (0.00164 - 0.09207) vs. 0.00110 (0.00015 - 0.00916)], and the difference was statistically significant (u=19.00, P<0.01). High LEF-1 expression predicted a significantly better overall survival in AML patients with intermediate-risk cytogenetics (χ2= 4.549, P= 0.033). Conclusions LEF-1 may be involved in the development and progression of AML at intermediate-risk patients and is closely related to tumor burden and treatment efficacy. LEF-1 may be a good predictor of better prognosis and a novel target for therapeutic effect.
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Objective To analyze the mRNA expression level of lymphoid enhance factor 1 (LEF-1), and to investigate its clinical significance in bone marrow mononuclear cells of patients with chronic myeloid leukemia chronic-phase (CML-CP) after initial diagnosis and chemotherapy, and to analyze its clinical significance. Methods The real-time fluorescence quantitative polymerase chain reaction was used to measure the expression level of LEF-1 gene in 38 CML-CP patients after initial diagnosis and chemotherapy and 20 persons without blood system diseases and neoplastic diseases as normal control. The difference of LEF-1 expression level between the patients and healthy control was compared, and the effect of imatinib on the main molecular response (MMR) was analyzed. Results The expression of LEF-1 mRNA in 38 newly diagnosed patients [0.00214 (0.00020 - 0.02120)] was significantly higher than that in normal controls [0.00101 (0.00009 - 0.00233)] (U= 163.0, P 0.05). The level of LEF-1 mRNA expression of non-MMR group was also higher than that of the normal control group (U= 14.0, P<0.01). The rate of acquiring MMR was significantly higher in high LEF-1 mRNA expression group [84.2 %(16/19)] than that in low expression group [47.4%(9/19)] (χ2=4.209, P<0.01). The time of acquiring MMR was significantly shorter in the high LEF-1 mRNA expression group [(10.0 ± 4.5) months] than that in the low expression group [(14.6 ± 3.8) months] (t= 2.705, P< 0.01). Conclusions LEF-1 may be involved in the occurrence and development of CML, and reflects the tumor burden. It may be one of the indicators to predict the efficacy of imatinib.
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Objective To investigate the mRNA level of lymphoid enhancing factor-1 ( LEF-1) in bone marrow mononuclear cells after the initial diagnosis and chemotherapy of patients with multiple myeloma (MM) and its clinical significance. Methods The LEF-1 mRNA of target gene in 42 MM patient was detected by real-time fluorescence quantitative polymerase chain reaction (RTQ-PCR), and 20 patients without hematological disease were enrolled as the healthy controls. Results The LEF-1 mRNA median level in previously diagnosed MM patients was significantly higher than that in the healthy controls [0.01068 (0.00017 - 0.14100) vs. 0.00101 (0.00009 - 0.002326)], and the difference was statistically significant (U = 91.00, P< 0.001); The LEF-1 mRNA median level in MM patients after chemotherapy was declined compared with the patients before chemotherapy [0.00011 (0.00001 - 0.01548) vs. 0.01068 (0.00017 -0.14100)], and the difference was statistically significant (U = 343.0, P< 0.001). The LEF-1 mRNA median level of MM patients after chemotherapy in progression of disease (PD) group was higher than that in the non-PD groups [0.08386 (0.00288 - 0.14100) vs. 0.003454 (0.000156 - 0.05660)], and the difference was statistically significant (U = 343.0, P< 0.001). The overall survival (OS) rate in the high LEF-1 expression group was shorter than that in the low LEF-1 expression group for MM patients in the initial diagnosis (47.6%vs. 65.5 %, χ2 = 3.931, P= 0.0414). Conclusion LEF-1 may be involved in the occurrence and development of MM, which has a potential to become an indicator of evaluating the poor prognosis and PD of MM patients, and could be served as a novel therapy target for the treatment of MM.
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Objective To explore the mechanism of drug resistance of ovarian cancer cells to TRAIL-induced apoptosis.Methods We collected 3AO cells and CAOV3 cells,respectively,at 18,24,48 and 72 hour under 12.5,25,50 and 100 ng/mL concentrations of TRAIL.The rate of cell growth inhibition was checked by methyl thiazolyl tetrazolium (MTT)assay to evaluate the effect of TRAIL.Morphology of apoptotic cells was observed by TdT-mediated-dUTP nick end labeling (TUNEL).The apoptosis rate was detected by flow cytometry (FCM)and C-FLIP protein was determined by Western blotting.Results TRAIL inhibited the growth of 3AO and CAOV3 cells.The rate of growth inhibition at 24 hour was 28% in 3AO cells and 10% in CAOV3 cells.TRAIL induced apoptosis of cells.The apoptosis rate at 24 hour was 8.5% in 3AO cells,which was higher than 5.5% in CAOV3 cells.The expression level of C-FLIP protein was higher in CAOV3 cells than in 3AO cells.Conclusion C-FLIP protein is an important protein that regulates drug resistance of ovarian cancer cells to TRAIL-induced apoptosis.
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<p><b>OBJECTIVE</b>To investigate the effects of 17β-estrogen on expressions of C-reactive protein (CRP) and its mRNA in vascular smooth muscle cells(VSMCs).</p><p><b>METHODS</b>Immunocytochemistry was used to detect CRP level in normal VSMCs. The expressions of C-reactive protein and p-ERK1/2 in Ang-II-stimulated VSMCs were evaluated with Western blot. C-reactive protein mRNA was examined with RT-PCR.</p><p><b>RESULTS</b>17β-estrogen had no effect on cell morphology and C-reactive protein expression in normal VSMCs; however, C-reactive protein and mRNA, as well as p-ERK1/2 were decreased in Ang-II-stimulated VSMCs after 17β-estrogen treatment in a concentration-dependent manner.</p><p><b>CONCLUSION</b>17β-estrogen may inhibit the expression of C-reactive protein and its mRNA in Ang-II-stimulated VSMCs via ERK1/2 signal transduction pathway in a concentration-dependent way.</p>