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Objective To investigate the impact of prescribed adaptive statistical iterative reconstruction V (Pre-ASiR-V) on imaging quality and radiation dosage of pure ground glass nodules (pGGN) in chest phantom,in order to obtain the optimal level of Pre-ASiR-V.Methods CT scanning for a chest phantom containing 4 artificial pGGNs was performed with Revolution CT,and the Pre-ASiR-V level was set as 0,20％,40％,60％,80％ and 100％ group,respectively.The mean noise,effective dose (ED) and the subjective scores of pGGN imaging were recorded and compared.Results The mean noise of groups (Pre-ASiR-V 0,20％,40％,60％,80％ and 100％) was (17.93±2.20)HU,(17.30±3.68)HU,(18.20± 3.44)HU,(18.80±0.20)HU,(19.87±2.56)HU and (15.90±4.56)HU,respectively (F=0.568,P=0.723).ED of these groups was 7.40 mSv,5.16 mSv,3.36 mSv,1.97 mSv,0.97 mSv and 0.33 mSv,respectively.Compared with imaging of PreASiR-V 0,the reduction percentage of ED was 30.27％,54.59％,73.38％,86.89％ and 95.54％,respectively.The subjective score of the image quality evaluated by the 2 observers had high agreement (Kappa=0.778,P=0.003),and all the scores were greater than 3.The subjective score of Pre-ASiR-V 80％ and 100％ group was slightly lower than those in other groups.Conclusion Different Pre-ASiR-V level slightly impacts the noise of high-resolution CT images of chest phantom,while reduces radiation dosage significantly.Pre-ASiR-V level of 60％ is the optimal protocol.
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Objective To compare the expression of nitric oxide synthase (NOS ) in patients with gastroesophageal reflex disease (GERD)and healthy controls.Methods The distribution and relative protein amount of two NOS subtypes (nNOS and iNOS)were determined with immunohistological method,and their mRNA levels were measured with real-time PCR method.Results The nNOS and iNOS were mostly distributed in the cytoplasm in epithelia of esophageal mucosa.The nNOS and iNOS in reflux esophagitis (RE)were significantly higher than in non-erosive reflux disease (NERD)patients and healthy controls (P <0.05 ).The mRNA levels of nNOS and iNOS were also significantly higher in RE patients than in NERD patients and healthy controls (P <0.05).Conclusion The expressions of nNOS and iNOS were increased in the esophagus of RE patients,which may be related to the effects of NO on the onset of GERD.
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<p><b>OBJECTIVE</b>To investigate the expression of Toll-like receptor 7 (TLR7) in gastric cancer cell lines and the effect of imiquimod, a TLR7 agonist, on the proliferation and apoptosis of SGC-7901 cells.</p><p><b>METHODS</b>The protein expression levels of TLR7 were detected with Western blotting in 3 human gastric cancer cell lines (SGC-7901, HGC-27 and MKN-28). The cell line expressing the highest TLR7 level was exposed to different doses of imiquimod for 12-72 h and the cell viability was assessed with MTT assay. The cell apoptosis rate after 100 µg/ml imiquimod treatment for 12 or 24 h was quantified by flow cytometry, and the ultrastructual changes of the cells were observed under electron microscope. The expression of apoptosis-related genes Bcl-2 and Bax were analyzed with real-time PCR.</p><p><b>RESULTS</b>All the 3 cell lines expressed TLR7, among which SGC-7901 cells showed the highest expression level. TLR7 agonist imiquimod dose- and time-dependently reduced the viability of SGC-7901 cells. Exposure to 100 µg/ml imiquimod for 24 h resulted in SGC-7901 cell apoptosis as shown by an increased ratio of early apoptotic cells and significant ultrastructural changes of the cells. Real-time PCR demonstrated that imiquimod treatment for 24 h caused a dose-dependent reduction of Bcl-2 mRNA expression and increment of Bax mRNA expression.</p><p><b>CONCLUSIONS</b>TLR7 protein is expressed in all the 3 gastric cancer lines and its agonist imiquimod can inhibit cell proliferation and induce apoptosis in SGC-7901 cells.</p>
Subject(s)
Humans , Aminoquinolines , Pharmacology , Apoptosis , Cell Line, Tumor , Cell Proliferation , Gene Expression Regulation, Neoplastic , Real-Time Polymerase Chain Reaction , Stomach Neoplasms , Metabolism , Pathology , Toll-Like Receptor 7 , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate the expression status of CXCR7 in gastric cancer tissues and cell lines.</p><p><b>METHODS</b>The expression status of CXCR7 was detected in 35 primary gastric cancer tissues and matched adjacent tissues by immunohistochemistry and RT-PCR. The correlation of CXCR7 expression with the clinicopathological parameters and risk factors of gastric cancer was analyzed. The expression of CXCR7 in gastric cell lines (HGC-27, MGC-803, BGC-823, SGC-7901 and MKN-28) was also detected by immunofluorescence assay.</p><p><b>RESULTS</b>The expression of CXCR7 was significantly higher in gastric cancer tissues than in adjacent tissues (P<0.01). CXCR7 expression was not correlated with age, gender, smoking history, Helicobacter pylori infection, tumor location or the pathological type, but showed a higher expression level in patients with a alcohol-drinking history than in those without (P<0.05). CXCR7 was expressed with variable intensities in the 5 gastric cancer cell lines without correlation with the degrees of cell differentiation; its expression was the highest in SGC-7901 cells, a moderately differentiated human gastric adenocarcinoma cell line.</p><p><b>CONCLUSIONS</b>CXCR7 is highly expressed in gastric cancer tissues with variable intensities in 5 gastric cancer cell lines, suggesting its important role in gastric cancer progression.</p>
Subject(s)
Humans , Cell Differentiation , Cell Line, Tumor , Disease Progression , Helicobacter Infections , Immunohistochemistry , Receptors, CXCR , Metabolism , Signal Transduction , Stomach Neoplasms , Diagnosis , MetabolismABSTRACT
<p><b>BACKGROUND</b>Pancreatic cancer is a common malignant tumor of the digestive system. It is the fourth major cause of tumor-related death and its morbidity is increasing, and hence it is imperative to develop effective forms of therapy for pancreatic cancer. Peptide tyrosine-tyrosine (PYY) is an important gastrointestinal peptide hormone. According to previous literatures, PYY has been shown to inhibit tumor proliferation in cellular and animal models, but there has been limited research on the detailed mechanism of PYY in pancreatic cancer. This study was to observe the effects of PYY on pancreatic cancer cell and investigate the possible mechanism.</p><p><b>METHODS</b>The expression of Y1, Y2, and Y5 receptors on pancreatic cancer cell lines were detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR). The cytotoxicity of PYY toward the MiaPaCa-2 cell was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay; the cell morphology and structure changes were observed under inverted microscope and transmission electron microscope respectively. Apoptosis and cell cycle were evaluated by flow cytometry. The activity of caspase-3 was determined by activity assay kits and Western blotting. The expression of survivin, vascular endothelial growth factor (VEGF), and cyclooxygenase-2 (COX-2) were determined by RT-qPCR and Western blotting.</p><p><b>RESULTS</b>Expression of Y2 receptor is the most abundant PYY receptor on pancreatic cancer cell. PYY inhibited MiaPaCa-2 cell proliferation, blocked it in G0/G1 phase, increased the proportion of apoptosis cells and caspase-3 activity, and reduced the expression of survivin, VEGF, and COX-2.</p><p><b>CONCLUSIONS</b>PYY weakened the ability of the pancreatic MiaPaCa-2 cell viability through cell cycle blocking and apoptosis inducing. The inhibition effect of PYY may be mediated by the Y2 receptor. The increased caspase-3 activity and reduced expression of survivin, VEGF, and COX-2 may serve as a novel mechanism in PYY inhibition effect on MiaPaCa-2 cell.</p>
Subject(s)
Humans , Blotting, Western , Caspase 3 , Genetics , Metabolism , Cell Cycle , Genetics , Cell Line, Tumor , Cell Proliferation , Cyclooxygenase 2 , Genetics , Metabolism , Dipeptides , Pharmacology , Inhibitor of Apoptosis Proteins , Genetics , Metabolism , Pancreatic Neoplasms , Genetics , Metabolism , Reverse Transcriptase Polymerase Chain Reaction , Vascular Endothelial Growth Factor A , Genetics , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate the therapeutic effect of thyroid hormone in nude mice bearing human pancreatic cancer xenograft.</p><p><b>METHODS</b>A BALB/c nude mouse model bearing pancreatic cancer was established with human pancreatic cancer cell line Bx-PC3. The mouse models were divided randomly into 5 groups, namely the control group treated with distilled water, high and low concentrations of thyroid hormone (T3) groups, and high and low concentration of propylthiouracil (PTU) groups. After intervention for 21 days, the changes in body weight and xenograft tumor volume and weight were measured, and the serum T3 concentration was detected by ELISA assay. The expression of proliferating cell nuclear antigen (PCNA) and microvessel density (MVD) were detected using immunohistochemistry.</p><p><b>RESULTS</b>The body weight of nude mice in T3 groups was significantly reduced after intervention, while that in PTU groups showed no obvious changes. Compared with PTU groups and control group, T3 groups showed significantly reduced tumor volume and weight (P<0.05) with also reduced PCNA expression and MVD, but these effect did not exhibit a dose dependence (P>0.05).</p><p><b>CONCLUSION</b>Thyroid hormone can inhibit the growth of human pancreatic cancer in nude mice by suppressing the proliferation and angiogenesis of the tumor cells, suggesting the potential value of thyroid hormone in pancreatic cancer therapy.</p>
Subject(s)
Animals , Humans , Male , Mice , Cell Line, Tumor , Mice, Inbred BALB C , Mice, Nude , Microvessels , Pathology , Neovascularization, Pathologic , Pancreatic Neoplasms , Pathology , Proliferating Cell Nuclear Antigen , Metabolism , Triiodothyronine , Pharmacology , Xenograft Model Antitumor AssaysABSTRACT
T polymorphism,was selected as putative promoter.The recombinant constructions containing-1328-+812 of TGF-?_1 gene and CAT reporter gene(phTGF2.14T,phTGF2.14C)were constructed and transfected into HepG2 cells with liposomal trans- fection method,then the transfected HepG2 cells were treated with IL-10(4 ng/ml),HGF(10 ng/ml)or IFN-?(20 ng/ml). Reporter gene activity was analyzed by ELISA.Results:Reporter gene activity in cells transfected with phTGF2.14C was sig- nificantly higher than those transfected with phTGF2.14T(P