Objective To evaluate the efficacy of anastomotic stenosis in upper gastrointestinal tract treated by balloon dilation under endoscopies and to analyze the causes of stenosis.Methods Balloon dilation under endoscopies was performed in 194 patients with anastomotic stenosis who had undergone esophagectomy or gastrectomy due to their malignancies. All patients were followed up for their symptoms, life quality and surviving times, and were regularly examined by endoscopies and esophageal barium radiography.Results The dysphagia in short term was completely released in 96 4% (187 of 194 patients). The average diameter of stoma was extended significantly from 0 44 cm to 2 36 cm after the therapy ( P

Mesaconitine was incubated with rat liver microsomes in vitro. The metabolites of mesaconitine in rat liver microsomes were identified by ultra performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) method with high resolution power. A typical reaction mixture of 100 mol L-1 Tris-HCI buffer (pH 7.4) containing 0.5 gL-1 microsomal protein and 50 micro molL-1 mesaconitine was prepared. The above reaction mixture was divided into six groups, and the volume of each group was 200 micro L. The incubation mixture was pre-incubated at 37 degrees C for 2 min and the reactions were initiated by adding NADPH generating system. After 90 min incubation at 37 degrees C, 200 micro L of acetonitrile was added to each group to stop the reaction. The metabolites of mesaconitine were investigated by UPLC-MS/MS method. Mesaconitine and 6 metabolites M1-M6 were found in the incubation system. The structures were characterized according to the data from MS/MS spectra and literatures. The metabolic reactions of mesaconitine in rat liver microsomes included the demethylation, deacetylation, dehydrogenation and hydroxylation. The major metabolic pathways of mesaconitine in rat liver microsomes were determined by UPLC-MS/MS on multiple reaction monitoring (MRM) mode combined with specific inhibitors of cytochrome P450 (CYP) isoforms, including alpha-naphthoflavone (CYP1A2), quinine (CYP2D), diethyldithiocarbamate (CYP2E1), ketoconazole (CYP3A) and sulfaphenazole (CYP2C), separately. Mesaconitine was mainly metabolized by CYP3A. CYP2C and CYP2D were also more important CYP isoforms for the metabolism reactions of mesaconitine, but CYP1A2 and CYP2E1 haven't any contribution to MA metabolism in rat liver microsomes.
Aconitine ; analogs & derivatives ; metabolism ; Animals ; Chromatography, High Pressure Liquid ; Cytochrome P-450 CYP3A ; metabolism ; Cytochrome P-450 CYP3A Inhibitors ; Cytochrome P-450 Enzyme Inhibitors ; Cytochrome P-450 Enzyme System ; metabolism ; Enzyme Inhibitors ; pharmacology ; Ketoconazole ; pharmacology ; Male ; Metabolic Networks and Pathways ; Microsomes, Liver ; enzymology ; metabolism ; Quinine ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Sulfaphenazole ; pharmacology ; Tandem Mass Spectrometry

Urokinase plasminogen activator receptor (uPAR) is a membrane protein which is attached to the cellular external membrane. The uPAR expression can be observed both in tumor cells and in tumor-associated stromal cells. Thus, in the present study, the human amino-terminal fragment (hATF), as a targeting element to uPAR, is used to conjugate to the surface of superparamagnetic iron nanoparticle (SPIO). Flowcytometry was used to examine the uPAR expression in different tumor cell lines. The specificity of hATF-SPIO was verified by Prussian blue stain and cell phantom test. The imaging properties of hATF-SPIO were confirmed in vivo magnetic resonance imaging (MRI) of uPAR-elevated colon tumor. Finally, the distribution of hATF-SPIO in tumor tissue was confirmed by pathological staining. Results showed that the three cells in which we screened, presented different expression characteristics, i. e., Hela cells strongly expressed uPAR, HT29 cells moderately expressed uPAR, but Lovo cells didn't express uPAR. In vitro, after incubating with Hela cells, hATF-SPIO could specifically combined to and be subsequently internalized by uPAR positive cells, which could be observed via Prussian blue staining. Meanwhile T2WI signal intensity of Hela cells, after incubation with targeted probe, significantly decreased, and otherwise no obvious changes in Lovo cells both by Prussian blue staining and MRI scans. In vivo, hATF-SPIO could be systematically delivered to HT29 xenograft and accumulated in the tumor tissue which was confirmed by Prussian Blue stain compared to Lovo xenografts. Twenty-four hours after injection of targeting probe, the signal intensity of HT29 xenografts was lower than Lovo ones which was statistically significant. This targeting nanoparticles enabled not only in vitro specifically combining to uPAR positive cells but also in vivo imaging of uPAR moderately elevated colon cancer lesions.
Cell Line, Tumor ; Colonic Neoplasms ; diagnosis ; Ferric Compounds ; Humans ; Magnetic Resonance Imaging ; Magnetite Nanoparticles ; chemistry ; Molecular Imaging ; methods ; Receptors, Urokinase Plasminogen Activator ; chemistry ; Staining and Labeling

Aged ; Antineoplastic Combined Chemotherapy Protocols ; adverse effects ; therapeutic use ; Carcinoma, Squamous Cell ; drug therapy ; radiotherapy ; Cisplatin ; administration & dosage ; adverse effects ; Combined Modality Therapy ; Esophageal Neoplasms ; drug therapy ; radiotherapy ; Esophagitis ; etiology ; Female ; Fluorouracil ; administration & dosage ; adverse effects ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Organoplatinum Compounds ; administration & dosage ; adverse effects ; Radiotherapy, Intensity-Modulated ; adverse effects ; Remission Induction ; Survival Rate ; Taxoids ; administration & dosage ; adverse effects ; Vomiting ; chemically induced

Adenocarcinoma ; pathology ; surgery ; Biopsy ; Diagnosis, Differential ; Gastric Fundus ; pathology ; surgery ; Humans ; Male ; Middle Aged ; Myelolipoma ; pathology ; surgery ; Neoplasms, Multiple Primary ; pathology ; surgery ; Pleural Neoplasms ; pathology ; surgery ; Stomach Neoplasms ; pathology ; surgery

Objective To report the clinical and myopathological features in a patient with common variable immunodeficiency (CVID) with myositis.Methods A 33 years old man suffered from recurrent respiratory infection with fever over 10 years.The symptoms improved after anti-infection therapy.At the same time he presented with fatigue.Two years ago he developed general muscle weakness,hypertrophy and myotonia,especially in the hands,neck and thighs.Genetic test for myotonic dystrophy protein kinase (DMPK) and zinc finger protein 9 (ZNF9) was performed.Laboratory tests,electromyography,muscle ultrasound and muscle biopsy were performed.In addition to standard histological and enzyme histochemical stainings,immunohistochemical method was used with primary antibodies of mouse anti human monoclonal antibodies including CD8 for T-lymphocytes,CD20 for B-lymphocytes,CD68 for macrophages and MHC-Ⅰ for muscle membrane.Results Electromyography revealed myogenic changes and abound with myotonic potentials.There was muscle hypertrophy in muscle ultrasound.Lung biopsy showed chronic inflammatory changes.Serum hypoimmunoglobulin and anemia were found.Muscle biopsy showed muscle fiber necrosis and regeneration with lymphocyte and macrophage infiltration.There were no gene mutations in DMPK and ZNF9 gene.Conclusion Muscle hypertrophy and myotonia appeared in CVID with myositis.

Objective To investigate the effects of exercise training(ET)on the expression of glucogen synthase kinase 3 bate(GSK 3?)in the adipose tissues of insulin resistant(IR)rats on a high fat diet(HFD). Methods Thirty male Wistar rats were randomly divided into a control group(n=10)and a model group(M group,n=20).Insulin resistance was established by feeding a HFD to the M group for 4 w,while rats in the control group were fed a normal diet.The IR rats were then randomly divided into two subgroups:an IR group and an ET group.All rats in the IR and ET groups were fed a HFD,but ET was administrated to the ET group for 6w.The expres- sion of GSK 3?protein in the rats'epididymis adipose tissue was detected using Western blotting,and body weight (BW),the concentrations of serum triglyceride and cholesterol(TG and TC),fasting plasma glucose(FPG)and serum insulin(FINS),as well as insulin sensitivity index(ISI)were regularly detected.Results Compared with the con- trol group,BW and the concentrations of serum TG and TC,FPG and FINS in the model group were significantly in- creased(P＜0.05),while ISI was decreased(P＜0.01).Compared with the control group,there was no difference in GSK 3 protein expression in the ET group,but the expression of GSK 3?protein in the ET group was obviously de- creased in comparison with that in the IR group(P＜0.05).Conclusion ET can ameliorate IR by decreasing GSK 3?protein expression in adipose tissues and enhancing the ingestion of glucose and the synthesis of glycogen.

BACKGROUND:Statins can promote the mRNA expression of bone morphogenetic protein 2, aggrecan and type II col agen in intervertebral disc cel s, and they also can reverse the phenotype of dedifferentiated nucleus pulposus cel s to slow disc degeneration process. OBJECTIVE:To review the research progress of simvastatin modulating the biological characteristics and mobilizing endogenous stem cel s for the repair of intervertebral disc degeneration. METHODS:The first author retrieved the PubMed and CNKI databases for relevant articles published before January 2016 using the key words of“disc degeneration factor, Simvastatin AND stem cel s, endogenous stem cel s AND disc degeneration”in English and Chinese, respectively. Initial y, 102 relevant articles were retrieved, but only 48 articles were included in result analysis fol owing elimination of duplicate studies.RESULTS AND CONCLUSION:By summarizing a large number of studies on the treatment of intervertebral disc degeneration worldwide, we found that simvastatin may modulate the biological characteristics and function of nucleus pulposus mesenchymal stem cel s via promoting the expression of hypoxia-inducible factor 1αfor the endogenous stem cel-based therapy of intervertebral disc degeneration.

Objective To construct and express human papillomavirus type 11(HPV11) E7 gene with recombinant adenovirus vectors. Methods HPV11 E7 gene was amplified by PCR and directionally cloned into vector pENTR-TOPO to form TOPO-E7 plasmid. E7 gene was transferred into the pAD/CMV/V5-DESTTM gateway vector by LR recombination reaction with pAD/CMV/V5-DESTTM gateway vectors and TOPO-E7 plasmid. The recombination vector was digested by Pac I enzyme and transfected into 293A cell by Lipofectamine method to obtain recombinant adenovirus vectors pAD-E7. Expression of E7 on HaCaT cells infected with pAD-E7 vectors was analyzed by confocal microscopy. Results The recombinant plasmid TOPO-E7 was identified and confirmed with enzyme digestion and sequencing. Recombinant adenovirus vectors pAD-E7 were generated efficiently with a titer of 1.4 ? 107 pfu/mL in transfected 293A cells. E7 protein could be identified in HaCaT cells with confocal microscope 48 h after infected with recombinant adenovirus vector. Conclusions The results indicate efficient expression of HPV11 E7 gene in eukaryotic cells by recombinant adenovirus mediated transfer, which facilitates further research of its function.