The capsule endoscope swallowed from the mouth into the digestive system can capture the images of important gastrointestinal tract regions. It can compensate for the blind spot of traditional endoscopic techniques. It enables inspection of the digestive system without discomfort or need for sedation. However, currently available clinical capsule endoscope has some limitations such as the diagnostic information being not able to correspond to the orientation in the body, since the doctor is unable to control the capsule motion and orientation. To solve the problem, it is significant to track the position and orientation of the capsule in the human body. This study presents an AC excitation wireless tracking method in the capsule endoscope, and the sensor embedded in the capsule can measure the magnetic field generated by excitation coil. And then the position and orientation of the capsule can be obtained by solving a magnetic field inverse problem. Since the magnetic field decays with distance dramatically, the dynamic range of the received signal spans three orders of magnitude, we designed an adjustable alternating magnetic field generating device. The device can adjust the strength of the alternating magnetic field automatically through the feedback signal from the sensor. The prototype experiment showed that the adjustable magnetic field generating device was feasible. It could realize the automatic adjustment of the magnetic field strength successfully, and improve the tracking accuracy.
Capsule Endoscopes ; Endoscopy ; Gastrointestinal Tract ; Humans ; Magnetic Fields

Objective:To investigate the effect of microRNA-146a (miR-146a) on apoptosis of human retinal microvascular endothelial cells (HRMECs) induced by high glucose and its possible molecular mechanism.Methods:HRMECs were cultured in vitro with 5.5 mmol/L D-glucose in the normal control group and 25 mmol/L D-glucose in the high glucose group for 48 hours, respectively.Normally cultured HRMECs were transfected by miR-146a mimics in the high glucose+ miR-146a mimics group or corresponding mimics control in the high glucose+ mimics control group by lipofection and cultured with 25 mmol/L D-glucose for 48 hours, respectively.Real-time fluorescent quantitative polymerase chain reaction (PCR) was performed to detect the expression level of miR-146a.MTT assay and flow cytometry were used to detect the activity and apoptosis of HRMECs, and Western blot was employed to detect the expression levels of apoptosis-associated protein B-cell lymphoma factor-2 (Bcl-2), Bcl-2 related X protein (Bax) and nuclear factor-κB (NF-κB) signaling-related proteins NF-κB p65 and p-NF-κB p65. Results:The relative expression levels of miR-146a were 1.00±0.10, 0.22±0.02, 0.21±0.02 and 0.88±0.09, and the cell viability was (100.00±10.06)%, (68.41±6.67)%, (67.91±6.74)% and (90.46±8.97)%, and the apoptosis rates were (3.11±1.02)%, (27.28±3.56)%, (27.44±4.03)% and (7.29±2.11)% in the normal control group, high glucose group, high glucose+ mimics control group and high glucose+ miR-146a mimics group, respectively.The relative expression levels of miR-146a and the cell viability were significantly lower, and the cell apoptosis rate was significantly higher in the high glucose group than those in the normal control group, with statistical significant differences (all at P<0.05). The relative expression levels of miR-146a and the cell viability were significantly higher, and the cell apoptosis rate was significantly lower in the high glucose+ miR-146a mimics group than those in the high glucose group and the high glucose+ mimics control group, and the differences were statistically significant (all at P<0.05). The relative expression levels of Bax and p-NF-κB p65 protein were significantly higher, the relative expression level of Bcl-2 protein was significantly lower in the high glucose group than those in the normal control group, showing statistically significant differences (all at P<0.05). The relative expression levels of Bax and p-NF-κB p65 protein were significantly lower, and the relative expression level of Bcl-2 protein was significantly higher in the high glucose+ miR-146a mimics group than those in the high glucose group and the high glucose+ mimics control group, and the differences were statistically significant (all at P>0.05). There was no significant difference in the relative expression of NF-κB p65 protein among the groups ( F=0.106, P=0.955). Conclusions:Overexpression of miR-146a may inhibit the apoptosis of HRMECs induced by high glucose, and its mechanism may be related to the inhibition of NF-κB signaling pathway activation.

Multi-modality imaging system based on fluorescence molecular tomography (FMT) has been widely used in animal studies.It combines FMT with other imaging modalities,which realizes the imaging of anatomical structure,physiological function and biological activities on molecular or cellular levels of small animal in vivo at the same time.This review gives an introduction to the history and current research status of singlemodality FMT system,introduces the developments of multi-modality system based on FMT,especially the system setup,working principle,performance and application of FMT/CT,FMT/MRI and FMT/radionuclide imaging.The prospects of multi-modality imaging system based on FMT are discussed.

Objectives To explore the calcium signaling mechanism of STIM1 in breast cancer cells. Meth-ods After SiRNA interruption, Western blot and Transwell were used to measure protein expression of STIM1 and cell migration in MDA-MB-231 cells respectively. The relationship between STIM1 and SOCE calcium signaling were analysed by Laser confocal microscopy. Western blots were used to measure protein expression of FAK after si-lence STIM1. Results The numbers of cells without STIM1 were significantly lower than those cells with STIM1 by Transwell assay. STIM1 mediated SOCE in MDA-MB-231. Blocking SOCE might inhibite cells migration. Si-lence STIM1 did not affect the expression or activation of FAK in MDA-MB-231 cells. Conclusion STIM1 influ-ences cell migration through SOCE pathway in breast cancer cells, which is independent on the expression or activa-tion of FAK.

Objective:To investigate the antitumor effect of CpG-ODN combining non-replicating recombinant vaccinia virus in tumor immunotherapy.Methods: CpG-ODN and constructed vaccinia virus v△11?75 were combined to study the antitumor effects in the walker′s rat tumor model.Results: Recombinant vaccinia virus v△11?75 lost the replicating capacity on human cell line,143TK - cell.The genes between HindⅢ C & K fragment of vaccinia virus TianTan strain were deleted,verified with Southern-blot. In the Walker′s tumor model of Wistar rats,Combinational immunotherapy with CpG-ODN and non-replicating vaccinia virus-modified WRC256 oncolysates resulted in prolonged life span and reduced tumor hyperplasia. Conclusion: CpG-ODN can enhance the antitumor effects of non-replicating vaccinia virus-modified oncolysates,providing a new route of tumor therapy.

AIM: To obtain a McAb that can inhibit the function of matrix metalloproteinase-2 (MMP-2), we expressed the fibronectin-like domain of MMP-2 (MFD) in vitro and prepared a McAb against MMP-2. METHODS: The purified MFD protein was used to immunize BALB/C mouse three times. Then the spleen of mouse was taken out and hybridized with hybridoma cells SP2/0. The positive cell clones were screened with ELISA method. The subtype and tissue specificity of the McAb were identified and its effect on endothelial cell migration and tube-formation was analyzed. RESULTS: After the spleen cells of the mouse and hybridoma cells SP2/0 were hybridized, a piece of cells that continuously secreted McAb against MMP-2 was obtained and named SZ-117. The titers of this McAb in culture supernatants and ascites were 2?10~-3 and 2?10~-5 , respectively. The heavy chain of the McAb belongs to IgG1 subclass. The McAb identified native MMP-2. MMP-2 existed in the stromal tissue of stomach, cholecystis, spleen, ovarian, prostate, salping and lymph node. It inhibited the invasion behavior of endothelial cells Eahy926 and pancreatic carcinoma cells 1990 and inhibited the tube-formation of Eahy926 cells. CONCLUSION: A useful tool for testing MMP-2 is obtained and it will be helpful to look for a kind of new anti-tumor material.

Objective To compare the diagnostic efficacies of narrow-band imaging (NBI) in distinguishing neoplastic from non-neoplastic colorectal lesions with routine endoscopy and with magnifying endoscopy. Methods Patients with colorectal lesions detected by NBI from September 2008 to February 2010 were enrolled in the study. These lesions were classified by pit pattern and capillary pattern, which was then assessed by reference to histopathology. Results A total of 100 patients with colorectal lesions were enrolled, and the lesions were observed by NBI with ordinary endoscopy (n =64) and NBI with magnifying endoscopy (n =36), respectively, and 7 cases (5 in NBI with ordinary endoscopy and 2 in NBI with magnifying endoscopy) which did not meet the diagnostic criteria were excluded. The overall diagnostic accuracy of NBI endoscopy in distinguishing neoplastic from non-neoplastic colorectal lesions was 91.4% ( 85/93 ), in which NBI with ordinary endoscopy and magnifying endoscopy was 89. 8% (53/59) and 94. 1% (32/34),respectively, with both significantly higher than that of conventional colonoscopy reported in the literature (79. 1% ) (P ＜ 0. 05 ). However, no significant difference was detected between 2 methods ( P ＞ 0. 05 ).Conclusion Similar with NBI magnifying endoscopy, NBI endoscopy without high magnification may also be useful to distinguish neoplastic from non-neoplastic colorectal lesions.

Objective To evaluate the effect of dexmedetomidine on the expression of nerve growth factor (NGF) in isolated hippocampal neurons of fetal rats incubated with propofol.Methods Hippocampal neurons derived from the fetal rats of pregnant Sprague-Dawley rats at 5-13 days of gestation were primarily cultured for 7 days,and were inoculated in the culture plate at a density of 5×105 cells/ml.The neurons were randomly divided into 3 groups (n =15 each) using a random number table:control group (group C),propofol group (group P),and dexmedetomidine + propofol group (group DP).In group P,propofol with the final concentration of 100 μmol/L was added to the culture medium,and the cells were incubated for 3 h.In group DP,dexmedetomidine with the final concentration of 1 μmol/L was added to the culture medium,the cells were incubated for 30 min,and then propofol with the final concentration of 100 μmol/L was added to the culture medium,and the cells were incubated for 3 h.The viability of hippocampal neurons was assessed by CCK-8 assay.NGF mRNA expression was detected by real-time reverse transcriptase polymerase chain reaction.NGF protein expression was detected by Western blot.Results Compared with group C,the viability of hippocampal neurons was significantly decreased,and the expression of NGF protein and mRNA was down-regulated in group P (P＜0.05).Compared with group P,the viability of hippocampal neurons was significantly increased,and the expression of NGF protein and mRNA was up-regulated in group DP (P＜0.05).Conclusion Dexmedetomidine improve propofol-induced decrease in the viability of isolated hippocampal neurons of fetal rats through up-regulating the expression of NGF.

OBJECTIVETo explore the molecular mechanism of microRNA-21 in myocardial damage of rats in the early stage of severe scald injury by observing the expression of microRNA-21 and programmed cell death 4 (PDCD4) in myocardial tissue of rat and to validate the relationship between them in cell model.

METHODS(1) Forty SD rats were divided into sham injury group (n =8, sham injured) and scald injury group (n =32, inflicted with 30% TBSA full-thickness scald on the back) according to the random number table. The left ventricular tissue was collected from rats in sham injury group at post injury hour 1 without any fluid infusion. Rats in scald injury group were given an intraperitoneal injection of lactic acid Ringer's solution and 8 rats were respectively sacrificed at post injury hour 3, 6, 12, 24 to harvest left ventricular tissue. The expression of microRNA-21 in myocardial tissue was assessed by real-time fluorescent quantitative RT-PCR. The protein expression of PDCD4 in myocardial tissue was assessed by Western blotting. (2) Rat myocardial cell line H9C2 was divided into microRNA-21 inhibitor group (cells were transfected with microRNA-21 inhibitor) and negative transfection control group (cells were transfected with negative control of microRNA inhibitor) according to the random number table. At post transfection hour 48, real-time fluorescent quantitative RT-PCR and Western blotting were performed respectively to determine the mRNA and protein expression levels of PDCD4 in cells. Data were processed with one-way analysis of variance, LSD-t and two independent samples t test. The relationship between microRNA-21 expression and PDCD4 protein level in myocardial tissue of rats was assessed by linear correlation analysis.

RESULTS(1) The expression levels of microRNA-21 in myocardial tissue of rats in sham injury group at post injury hour 1 and in scald injury group at post injury hour 3, 6, 12, 24 were respectively 0. 96 ± 0. 13, 0. 44 ± 0. 08, 0. 42 ± 0. 10, 0.33 +0.07, and 0.61 0.10 (F = 27.331, P <0.001). Compared with that in myocardial tissue of rats in sham injury group at post injury hour 1, expression level of microRNA-21 was significantly decreased in scald injury group at post injury hour 3, 6, 12, 24 (with t values from 4. 558 to 9.410, P values below 0.01). The protein expression levels of PDCD4 in myocardial tissue of rats in sham injury group at post injury hour 1 and in scald injury group at post injury hour 3, 6, 12, 24 were respectively 0.44 ± 0.05, 0.60 ± 0.09, 0.92 ± 0. 15, 0. 86 ± 0.11, and 0.57 ± 0. 10 (F =8.622, P =0.003). Compared with that in sham injury group at post injury hour 1, protein expression level of PDCD4 was significantly increased in scald injury group at post injury hour 6 and 12 (with t values respectively 4. 968 and 4. 122, P values below 0.01). A significant negative correlation between the expression of microRNA-21 and PDCD4 protein in myocardial tissue of rats of scald injury group was observed at each time point (r = -0. 572, P = 0. 026). (2) The mRNA and protein expression levels of PDCD4 of myocardial cells in microRNA-21 inhibitor group were respectively 1.73 ± 0. 29 and 0. 38 ± 0. 08, which were significantly higher than those in negative transfection control group (0.95 ± 0.14 and 0.23 ± 0.03, with t values respectively 4. 857 and 3.356, P <0.05 or P <0.01).

CONCLUSIONSExpression of microRNA-21 was decreased, while expression of PDCD4 was increased, in myocardial tissue of rats in the early stage of severe scald injury. MicroRNA-21 might participate in myocardial damage in the early stage of scald injury by negatively regulating expression of PDCD4.

Animals ; Apoptosis Regulatory Proteins ; metabolism ; Blotting, Western ; Burns ; metabolism ; pathology ; MicroRNAs ; genetics ; metabolism ; Myocardium ; metabolism ; pathology ; Myocytes, Cardiac ; metabolism ; pathology ; Rats ; Reverse Transcriptase Polymerase Chain Reaction ; Soft Tissue Injuries

Objective To observe the therapeutic effect and toxicity reaction of Oxaliplatin com- bined with XeLoda in the treatment of 42 patients with advanced colorectal cancer.Methods All the pa- tients were treated with Oxaliplatin(130 mg/m~2,ivgtt for 2 h,d1)combined with XeLoda(2000 mg?m~(-2)?d~(-1), po,bid,d1 to d14).The regime was repeated every 21 days for at least 3 consecutive cycles.Results The to- tal response rate was 40.5%(17/42)in which 2 got CR and 15 PR.24 patients got Kamofsky score increased. The major toxic effects were alopecia,peripheral neuritis,gastrointestinal tract reactions and myelosuppression. Conclusion Oxaliplatin combined with XeLoda regimen is effective in the treatment of advanced colorectal cancer,and its toxicity is tolerable.It is worth studying in the future.