The technique introduced in this paper is applied in the endocardial catheter operation, which describes the 3D heart model reconstruction before the operation for the endocardial navigation. After a series of CT images of the thorax are processed, an accurate 3D endocardial model can be reconstructed. At first, the series of 2D CT images are preprocessed for denoising and the enhancement,then they are constructed as the volume data. After the region growing segmentation in the 3D volume data according to the grey value of the voxel in the heart cavity, the heart surface rendering is got and the 3D model of endocardial cavity is reconstructed.
Cardiac Catheterization ; methods ; Imaging, Three-Dimensional ; Models, Cardiovascular ; Tomography, X-Ray Computed ; methods

OBJECTIVETo investigate the estrogen-like activities of icariin (ICA), icaritin (ICT) and desmethylicaritin (DICT) and their structure/activity relationships.

METHODSICT was hydrolyzed from ICA by cellulase and then DICT was demethylated from ICT in boron tribromide and dichloromethane system. Estrogen-sensitive MCF-7 cells and T47D cells were co-incubated with different concentrations of test compounds for 6 and 9 d respectively, and the cell proliferation was measured by MTT.

RESULTSICT and DICT both markedly enhanced cell proliferation. Compared with estradiol (10.(-9) mol/L), the proliferative effects of 10.-6 mol/L ICT and DICT on MCF-7 cells were 90.0% and 94.0% (P<0.01), respectively, and those of T47D cells were 65.6% and 50.0%. (P<0.01). But this phenomenon was not observed with ICA. Cell proliferation induced by ICT and DICT was completely antagonized by 10.(-7 )mol/L pure estrogen receptor antagonist, ICI182,780.

CONCLUSIONICT and DICT possess estrogen-like activity of enhancing proliferation in MCF-7 and T47D cells. However, ICA appears to have no estrogenicity on MCF-7 and T47D cell lines in vitro.

Breast Neoplasms ; pathology ; Cell Division ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Flavonoids ; chemistry ; pharmacology ; Humans ; Phytoestrogens ; isolation & purification ; pharmacology ; Tumor Cells, Cultured

Objective To further investigated the effect of minocycline on the inhibition of microglial activation and subsequent protection of nigral DA neuron.Methods 20 rats injected with LPS in the substantia nigra (SN) were randomly divided into two groups (LPS group and LPS+Minocycline group).The behavior was observed on the 7~(th) d and 14~(th) d.The immunohistoehemistry,in situ hybridization and Western-blot were used to detect the levels of positive neuron,mRNA,protein of TH and OX-42. Results The slightly rotational behavior was observed in LPS+Minoeyeline group.The majority of mieroglias were activated in the two groups.Some microglia in the SNpc remained ramified in LPS+ Minocycline group.The numbers of hypertophie microglia in LPS+Minoeyeline group were less than that in LPS group.Western-blot showed that the protein of OX-42 in two LPS groups was higher than in normal group(P

It is now well established that inflammation plays an important role in the development of numerous chronic metabolic diseases including insulin resistance (IR) and type 2 diabetes (T2DM). Skeletal muscle is responsible for 75% of total insulin-dependent glucose uptake; consequently, skeletal muscle IR is considered to be the primary defect of systemic IR development. Our pre- vious study has shown that rutaecarpine (Rut) can benefit blood lipid profile, mitigate inflammation, and improve kidney, liver, pan- creas pathology status of T2DM rats. However, the effects of Rut on inflammatory cytokines in the development of IR-skeletal muscle cells have not been studied. Thus, our objective was to investigate effects of Rut on inflammatory cytokines interleukiri (IL)-1, IL-6 and tumor necrosis factor (TNF)-α in insulin resistant primary skeletal muscle cells (IR-PSMC). Primary cultures of skeletal muscle cells were prepared from 5 neonate SD rats, and the primary rat skeletal muscle cells were identified by cell morphology, effect of ru- taecarpine on cell proliferation by MTT assay. IR-PSMC cells were induced by palmitic acid (PA), the glucose concentration was measured by glucose oxidase and peroxidase (GOD-POD) method. The effects of Rut on inflammatory cytokines IL-1, IL-6 and TNF-α in IR-PSMC cells were tested by enzyme-linked immunosorbent assay (ELISA) kit. The results show that the primary skeletal muscle cells from neonatal rat cultured for 2-4 days, parallel alignment regularly, and cultured for 7 days, cells fused and myotube formed. It was shown that Rut in concentration 0-180. 0 μmol x L(-1) possessed no cytotoxic effect towards cultured primary skeletal muscle cells. However, after 24 h exposure to 0.6 mmol x L(-1) PA, primary skeletal muscle cells were able to induce a state of insulin resistance. The results obtained indicated significant decrease (P < 0.05 to P < 0.001) IL-1, IL-6 and TNF-α production by cultured IR-PSMC cells when incubating 24 hours with Rut, beginning from 20 to 180.0 μmol x L(-1). IL-1, IL-6 and TNF-α in the Rut treated groups were dose-dependently decreased compared with that in the IR-PSMC control group. Our results demonstrated that the Rut promoted glucose consumption and improved insulin resistance possibly through suppression of inflammatory cytokines in the IR-PSMC cells.
Animals ; Cell Proliferation ; drug effects ; Cytokines ; metabolism ; Female ; Glucose ; metabolism ; Indole Alkaloids ; pharmacology ; Inflammation ; metabolism ; Insulin Resistance ; Male ; Muscle, Skeletal ; cytology ; drug effects ; metabolism ; Quinazolines ; pharmacology ; Rats

This research is to study the relationship between HPLC fingerprints of Moutan Cortex, Paeoniae Radix Rubra and Paeoniae Radix Alba and their activity on lipopolysaccharide-induced acute lung injury. HPLC fingerprints of each extract of Moutan Cortex,Paeoniae Radix Rubra and Paeoniae Radix Alba were established by an optimized HPLC-MS method. The activities of all samples against protein and tumor necrosis a factor were tested by the model of lipopolysaccharide-induced acute lung injury. The possible relationship between HPLC-MS fingerprints and the activitieswere deduced by the Partial least squares regression analysis method. Samples were analyzed by HPLC-MS/MS to identify the major peaks. The results showed that each sample had some effect on acute lung injury. Four components with a lager contribution rate of efficacy were calculated by the research of spectrum-effect relationship. Moutan Cortex exhibited good activity on acute lung injury, and gallic acid, paeoniflorin, galloylpaeoniflorin and paeonol were the main effective components.
Acetophenones ; chemistry ; pharmacology ; Acute Lung Injury ; chemically induced ; drug therapy ; Animals ; Bridged Bicyclo Compounds, Heterocyclic ; chemistry ; pharmacology ; Chromatography, High Pressure Liquid ; methods ; Drugs, Chinese Herbal ; chemistry ; pharmacology ; Gallic Acid ; chemistry ; pharmacology ; Glucosides ; chemistry ; pharmacology ; Lipopolysaccharides ; pharmacology ; Male ; Monoterpenes ; chemistry ; pharmacology ; Paeonia ; chemistry ; Plant Roots ; chemistry ; Rats ; Rats, Wistar ; Tandem Mass Spectrometry ; methods

Objective To explore the possible mechanisms of Galectin - 1(Gal - 1)protein in promoting the invasion and migration of gastric cancer cells. Methods After treated with different concentrations(0,1,5 μg/ mL)of Gal - 1 protein, the Trans - well model was used to analyze the invasion and migration ability of gastric cancer. WB and gelatin zymography method were used to detect the MMP - 9 expression and active form change in gastric cancer cells after Gal - 1 stimulate, in order to explore the possible molecular mechanisms of Gal - 1 protein in promoting the invasion and migration of gastric cancer cells. Results In cell migration assay,the number of gastric cancer cells BGC - 823 treated with 1and 5 μg/ mL Gal - 1 stimulate were 117 ± 8. 19 and 167 ± 7. 55,higher than that treated with 0 μg/ mL(P < 0. 05). The number of gastric cancer cells 7 901 treated with 1and 5 μg/ mL Gal - 1 stimulate were 151 ± 5. 13 and 190. 3 ± 6. 8,higher than that treated with 0 μg/ mL(P < 0. 05). In cell invasion assay,the number of gastric cancer cells BGC - 823 treated with 1and 5μg/ mL Gal - 1 stimulate were 51 ± 3. 6 and 76. 7 ± 9. 07,higher than that treated with 0 μg/ mL(P < 0. 05). The number of gastric cancer cells 7 901 treated with 1and 5 μg/ mL Gal - 1 stimulate were 74. 0 ± 7. 21 and 105. 3 ± 11. 37,higher than that treated with 0 μg/ mL(P < 0. 05). The migration and invasion level were significantly increased in gastric cancer cells after Gal - 1 stimulate. The MMP - 9 expression level and active form change in gastric cancer cells were also increased after Gal - 1 stimulate. Conclusion Gal - 1cound significantly promote gastric cancer cell migration and invasion by up - regulated the MMP - 9 expression and active its enzyme activity.

OBJECTIVEIn order to explore pathogenic mechanism of laryngeal carcinoma, the involved genes were identified in larynx carcinogenesis by comparing the gene expression profile in matched primary normal epithelial cells and primary laryngeal carcinoma cells from the same patients.

METHODSA cDNA microarray analysis consisting of 11,431 human genes revealed significant changes in the expression of 35 genes, with 8 genes being up-regulated and 27 being down-regulated. The epithelial membrane protein-1 (EMP-1) is one of the down-regulated genes. EMP-1 expression in various kinds of laryngeal carcinoma was determined by semi-quantitative reverse transcriptase polymerase chain reaction (qRT-PCR).

RESULTSThe EMP-1 mRNA levels in all laryngeal carcinoma cells was significantly lower than that in the matched primary normal epithelial cells (P < 0.05) and were not correlated to the stage and differentiation of laryngeal carcinoma (P > 0.05).

CONCLUSIONSThe EMP-1 expression was correlated to larynx carcinogenesis and may be helpful to elucidate the pathogenic mechanism in laryngeal carcinoma.

Adult ; Aged ; Female ; Humans ; Laryngeal Neoplasms ; genetics ; metabolism ; Male ; Middle Aged ; Neoplasm Proteins ; Oligonucleotide Array Sequence Analysis ; Receptors, Cell Surface ; biosynthesis ; genetics ; Reverse Transcriptase Polymerase Chain Reaction

OBJECTIVEThis study was to explore the cytotoxic effect and the related injury mechanism of deoxynivalenol (DON) on articular chondrocytes in human embryo.

METHODSArticular cartilage cells were isolated from knees of human embryo and cultured in DMEM/F12 medium. The cells of the 4th generation were divided into five groups and incubated with varying concentrations of DON as the followings: control group and group with DON of 0.1, 0.2, 0.4, 1.0 µg/ml. The effects of DON were observed 72 hours after incubation. Cell apoptosis was assayed by flow cytometry (FCM) with Annexin V-FITC/PI staining; MMP-13 and PGE2 were detected by ELISA kits; NO was measured by Griess assay with spectrophotometer. Inducible nitric oxide synthase (iNOS) and collagen II in cells were detected by FCM. The expression levels of iNOS, mRNA and collagen II mRNA were measured with RT-PCR.

RESULTSThe rates of cell apoptosis in DON groups were 6.78% - 19.05%, which were significantly higher than that in control (1.20%, F = 174.761, P < 0.05). The levels of NO in DON groups were 20.8 - 40.7 µmol/L, which were significantly higher than that in control (10.2 µmol/L, F = 91.966, P < 0.05). The levels of MMP-13 in DON groups were 0.25 - 0.56 µmol/L, which were significantly higher than that in control (0 µmol/L, F = 78.420, P < 0.05). The levels of PGE2 in DON groups were 3.2-20.6 µmol/L, which were significantly higher than that in control (11.6 µmol/L, F = 276.453, P < 0.05). The proportions of cells with positive iNOS in DON groups were 14.8% - 56.8% which were significantly higher than that in controls (7.1%, F = 214.614, P < 0.05). The proportions of cells with positive collagen II in groups with DON of 0.4 µg/ml and 1.0 µg/ml were 56.7% and 52.7%, which were significantly lower than that in control (62.2%, F = 5.134, P < 0.05). The relative absorbance values of iNOS mRNA in DON groups were 1.07 - 1.33, which were significantly higher than that in control (0.62, F = 8.358, P < 0.05). The levels of collagen II mRNA in groups with DON of 0.4 µg/ml and 1.0 µg/ml were 0.83 and 0.82, which were significantly lower than that in control (1.14, F = 7.887, P < 0.05).

CONCLUSIONDON could promote anabolism of NO in articular cartilage cells by which up-regulated the expression of PGE2 and MMP-13, which both promoted resolution of articular cartilage matrix such as collagen II. DON induced apoptosis in articular cartilage cells.

Cartilage, Articular ; cytology ; embryology ; Cells, Cultured ; Chondrocytes ; drug effects ; metabolism ; Dinoprostone ; metabolism ; Humans ; Matrix Metalloproteinase 13 ; metabolism ; Nitric Oxide ; biosynthesis ; Trichothecenes ; toxicity

In this paper, a method based on the convex hull algorithm is presented for extracting modelling data from the locations of catheter electrodes within a cardiac chamber, so as to create a 3-D model of the heart chamber during diastole and to obtain a good result in the 3-D reconstruction of the chamber based on VTK.
Algorithms ; Body Surface Potential Mapping ; methods ; Catheter Ablation ; Humans ; Image Processing, Computer-Assisted ; methods

OBJECTIVETo investigate the effects of tetramethylpyrazine on lipopolysaccharides (LPS)-induced expression of vascular endothelial growth factor (VEGF) and hypoxia-induced factor-1alpha (HIF-1alpha) in macrophages.

METHODRat peritoneal macrophages were treated with LPS, and at the same time given different doses of tetramethylpyrazine. The secreation of VEGF was determined by ELISA test, and MTT assay was used to examine cells proliferation. Western blot assay was used to examine the expression of HIF-1alpha.

RESULT100 microg x mL(-1) and 10 microg x mL(-1) tetramethylpyrazine decreased the secretion of VEGF and also inhibited the expression of HIF-1alpha by LPS-induced macrophages. But these doses of tetramethylpyrazine had no effect on the cells proliferation.

CONCLUSIONTetramethylpyrazine could inhibit the secretion of VEGF by LPS-induced macrophages, and the mechanism must be associated with inhibiting the expression of HIF-1alpha. The inhibition effect was not due to inhibition of the proliferation of macrophages.

Animals ; Cell Proliferation ; drug effects ; Cells, Cultured ; Hypoxia-Inducible Factor 1, alpha Subunit ; metabolism ; Ligusticum ; chemistry ; Macrophages, Peritoneal ; cytology ; metabolism ; Male ; Plants, Medicinal ; chemistry ; Pyrazines ; isolation & purification ; pharmacology ; Rats ; Rats, Wistar ; Vascular Endothelial Growth Factor A ; biosynthesis