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By making use of 19 keywords,the paper searches the APP Store for APP related to imaging diagnostics and interventional radiology,analyzes parameters like APP classifications,satisfaction,publisher identity and downloads with statistical methods.The result shows that mobile learning APP,which facilitate imaging diagnostics and interventional radiology doctors with mobile learning,are more popular.
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OBJECTIVE@#To prepare ion exchange doxorubicin-loaded poly (acrylic acid) microspheres (DPMs) and evaluate the properties of these chemoembolic agents.@*METHODS@#Poly (acrylic acid) microspheres (PMs) without drug were prepared by inverse suspension polymerization method and then doxorubicin was loaded by ion exchange mechanism to prepare DPMs. Optical microscope was used to investigate the morphology and particle size distribution of PMs and DPMs; fluorescence microscope and confocal microscope were used to observe the distribution of doxorubicin after drug loading. Elasticities of both the microspheres were evaluated by texture analyzer. High performance liquid chromatography (HPLC) method was established to determine the drug loading behavior of PMs and releasing behavior of DPMs. The in vivo embolic property was evaluated by embolizing the hepatic artery of a rabbit with 0.1 mL of DPMs.@*RESULTS@#PMs and DPMs were both spherical in shape, smooth in surface and dispersed well. Doxorubicin was mainly in the outer area inside of DPMs and distributed evenly. The average particle size of PMs and DPMs were (283±136) μm and (248±149) μm, respectively. PMs and DPMs both had good compression ability with the Young's modulus of (62.63±1.65) kPa and (93.94±1.10) kPa separately. PMs reached the drug loading balance at 12 h, and the entrapment efficiency was greater than 99%. Drug loading of PMs in doxorubicin solution at the concentration of 5.0 g/L and 12.5 g/L was (19.78±0.27) g/L and (49.45±0.37) g/L, respectively. Doxorubicin released slowly from DPMs in PBS and the accumulative release percentages of DPMs with corresponding drug loading were 6.82%±0.02% and 2.83%±0.10% after 24 h, respectively. Arterial angiograms showed that the hepatic artery of the rabbit was successfully embolized with DPMs.@*CONCLUSION@#DPMs with good performance of loading doxorubicin could be a potential embolic agent for transcatheter arterial chemoembolization.
Subject(s)
Animals , Rabbits , Acrylates , Doxorubicin/administration & dosage , Embolization, Therapeutic/methods , Microspheres , Particle SizeABSTRACT
<p><b>OBJECTIVE</b>To clarify the role of mast cells and neuropeptides substance P (SP), somatostatin (SS), and vasoactive intestinal peptide (VIP) in dextran sulfate sodium (DSS)-induced colitis in rats.</p><p><b>METHODS</b>Experimental colitis was induced in Sprague-Dawley rats (180-200 g, n=20) by oral ingestion of 4% (w/v) DSS in drinking water for 7 days. Control rats (n=5) drank water and were sacrificed on day 0. Mast cell number, histamine levels in whole blood and tissue, tissue levels of SP, SS and, VIP in the distal colon of the rats were measured on day 8, day 13, and day 18 of experimentation.</p><p><b>RESULTS</b>Oral administration of 4% DSS solution for 7 days resulted in surface epithelial loss and crypt loss in the distal colon. Mast cell count increased on day 8 (1.75±1.09/mm vs. 0.38±0.24/mm, P<0.05) and day 13 (1.55±1.01/mm vs. 0.38±0.24/mm, P<0.05) after DSS treatment. Whole blood histamine levels were increased on day 8 (266.93±35.62 ng/mL vs. 76.87±32.28 ng/mL, P<0.01) and gradually decreased by day 13 and day 18 after DSS treatment. Histamine levels in the distal colon were decreased on day 8 (1.77±0.65 ng/mg vs. 3.06±0.87 ng/mg, P<0.05) and recovered to control levels by day 13 after DSS treatment. SP level in the distal colon gradually increased and were raised significantly by day 13 (8777.14±3056.14 pg/mL vs. 4739.66±3299.81 pg/mL, P<0.05) after DSS treatment. SS and VIP levels in the distal colon were not changed.</p><p><b>CONCLUSIONS</b>Mast cell degranulation followed by histamine release may play an important role in the pathogenesis of colitis induced by DSS. SP may be a significant substance in the progression of inflammation and the recovery process of DSS-induced colitis.</p>
Subject(s)
Animals , Male , Rats , Colitis , Pathology , Dextran Sulfate , Histamine , Mast Cells , Physiology , Neuropeptides , Physiology , Rats, Sprague-Dawley , Somatostatin , Substance P , Vasoactive Intestinal PeptideABSTRACT
<p><b>BACKGROUND</b>Different strategies for hepatocellular carcinoma (HCC) may have distinct effects on the immune system. The aim of this research was to investigate changes in the immunological function after transcatheter arterial chemoembolization (TACE) plus radiofrequency ablation (RFA) in HCC patients.</p><p><b>METHODS</b>A total of 51 consecutive HCC treatment-naïe patients was enrolled in this study and 20 healthy subjects served as controls. The therapeutic strategy was selected according to the tumor stage and general conditions. TACE was performed in 25 cases, TACE plus RFA in 17 and RFA in nine. All the patients underwent routine examinations and peripheral blood was harvested for the detection of lymphocyte subset by flow cytometry 1 day before, and 2 and 4 weeks after the treatment. The serum levels of alpha-fetoprotein (AFP), ALT and AST were also measured before and 4 weeks after treatment for the evaluation of therapeutic efficacy and liver function impairment.</p><p><b>RESULTS</b>When compared with healthy controls, the CD4/CD8 ratio and the number of B cells and natural killer (NK) cells were significantly decreased in HCC patients before treatment (P < 0.05). When compared with before treatment, the CD4+ cells and CD4/CD8 ratio decreased but CD8+ cells increased in the TACE group (P < 0.05); the CD4/CD8 ratio and NK cells decreased but CD8+ cells increased in the TACE-RFA group (P < 0.05); the CD3+ cells, CD4+ cells, CD4/CD8 ratio and NK cells increased in the RFA group (P < 0.05). Significant differences in the CD3+ cells, CD8+ cells, CD4/CD8 ratio and NK cells were observed among groups (P < 0.05). Moreover, the AFP level decreased and transaminase level increased in all groups (P < 0.05). Differences of pre and post treatment between groups were statistically significant (P = 0.016, 0.025, 0.018 respectively).</p><p><b>CONCLUSIONS</b>Immunity was compromised in HCC patients; TACE and TACE plus RFA lowered immunologic function to a certain extent. RFA improved it accompanied by a protective effect on liver function.</p>
Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , CD4-CD8 Ratio , Carcinoma, Hepatocellular , Allergy and Immunology , Therapeutics , Catheter Ablation , Chemoembolization, Therapeutic , Methods , Combined Modality Therapy , Killer Cells, Natural , Allergy and Immunology , Liver Neoplasms , Allergy and Immunology , Therapeutics , alpha-FetoproteinsABSTRACT
<p><b>OBJECTIVE</b>To investigate the role of mast cells and gut hormones and their interactions in TNBS-induced ulcerative colitis.</p><p><b>METHODS</b>Rat models of ulcerative colitis were established by a single intracolonic injection of 100 mg/kg TNBS (in 0.3 ml 50% ethanol). At 0, 6, 11, 16, 21 days after TNBS injection, the rats were sacrificed to determine the count of the mast cells. Histamine level in the whole blood, and the levels of histamine, substance P (SP), vasoactive intestinal peptide (VIP), and somatostatin (SS) in the distal colons were measured by fluorimetry or radioimmune assay. Immunofluorescence double staining was used to observe the relationship of the mast cells with SP, VIP, and SS positive nerve fibers.</p><p><b>RESULTS</b>On day 6 after TNBS injection, obvious ulcers occurred in the distal colon of the rats with significantly increased histamine level in the whole blood (P<0.05) but significantly decreased colonic histamine levels (P<0.05). The histamine levels in the whole blood and distal colon gradually recovered the normal levels. The mast cells significantly increased on day 16 (P<0.05) and maintained the high level till day 21. The distribution of mast cells was altered after TNBS injection, and the cells were found to aggregate in the myenteric region. SP levels in the distal colon significantly increased on day 11 (P<0.05) and maintained the high level till day 21. Immunofluorescence double staining revealed numerous mast cells close to the SP- and VIP-positive nerve fibers at different time points after TNBS injection. VIP positivity and the number of VIP-positive nerve fibers in the myenteric region were markedly increased, but no mast cells were observed in association with SP- and VIP-positive nerve fibers. The distribution of MC was not found to associate with the SS-positive nerve fibers.</p><p><b>CONCLUSION</b>The mast cells and histamine released by them, as well as parasecretion of SP and VIP, participate in tissue damage by TNBS-induced colitis. Bidirectional neuroimmunomodulation of the mast cells, SP and VIP have important effect on the development of TNBS-induced colitis.</p>
Subject(s)
Animals , Male , Rats , Colitis, Ulcerative , Metabolism , Pathology , Disease Models, Animal , Mast Cells , Bodily Secretions , Rats, Sprague-Dawley , Substance P , Metabolism , Trinitrobenzenesulfonic Acid , Toxicity , Vasoactive Intestinal Peptide , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate the mechanism of gastric carcinoma cells apoptosis induced by matrine injection in vitro.</p><p><b>METHODS</b>Effects of 24, 48, 72, 96 h incubation with different concentrations (0.25-1.5 g/L) of matrine injection on proliferation of SGC-7901 cells were evaluated using 3-4,5-dimethylthiazol-2-yl-2,5-diphenyltetrazolium bromide (MTT) assay. The cellular morphology of SGC-7901 cells was observed by transmission electron microscope (EM). Flow cytometry was used to analyze the apoptosis of SGC-7901 cells by staining with annexin V-FITC/PI. The expression of Fas/FasL was examined by flow cytometry using specific antibody. The activity of caspase-3 was measured by spectrofluorometry.</p><p><b>RESULTS</b>Matrine injection could inhibit the proliferation of SGC-7901 cells in a dose- and time-dependent manner. The typical morphological changes of apoptosis were observed after incubation with 1.0 g/L matrine injections for 48 h. The apoptosis rates of 0.5 g/L, 1.0 g/L and 1.5 g/L groups were 39.80%, 58.11% and 79.00% respectively. The apoptotic cells in matrine injection group were mainly early apoptotic cells, and those in 5-FU group were mainly late apoptotic cells and necrotic cells. Spectrofluorometry revealed FI levels of Fas and FasL were equal, which were both correlated with apoptosis rate. The activity of caspase-3 increased with the elevation of matrine concentration, and was correlated with the apoptosis rate.</p><p><b>CONCLUSION</b>Matrine injection can induce apoptosis of SGC-7901 cells through the up-regulation of Fas/FasL expression and activation of caspase-3.</p>
Subject(s)
Humans , Alkaloids , Pharmacology , Antineoplastic Agents, Phytogenic , Pharmacology , Apoptosis , Caspase 3 , Metabolism , Cell Line, Tumor , Fas Ligand Protein , Metabolism , Proto-Oncogene Proteins c-bcl-2 , Metabolism , Quinolizines , Pharmacology , Stomach Neoplasms , Up-Regulation , fas Receptor , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To construct an expression vector of small interfering RNA (siRNA) against survivin and observe its effects on survivin expression and proliferation of human pancreatic cancer cell line PC-2 and breast cancer cell line MCF-7.</p><p><b>METHODS</b>Constructed an expression vector of siRNA against survivin and transfected it into PC-2 and MCF-7 cells using lipofectamine 2000. The expression of survivin was detected by semi-quantitive RT-PCR and immunohistochemistry, and its effects on proliferation of PC-2 and MCF-7 cells were detected by MTT assay.</p><p><b>RESULTS</b>The introduction of sequence-specific siRNA could efficiently suppress survivin expression at both mRNA and protein levels in the two cancer cell lines. In PC-2 cells, the expression inhibition rates were 81.25% at mRNA level and 74.24% at protein level. In MCF-7 cells, the expression inhibition rates were 64.91% at mRNA level and 79.72% at protein level. The proliferation of PC-2 and MCF-7 cells was also suppressed, and 24 and 48 hours after the cells were reseeded, the proliferation inhibition rates of PC-2 cells were 28.00% and 33.38%, and that of MCF-7 cells were 31.58% and 33.02%, respectively.</p><p><b>CONCLUSIONS</b>The expression vector of siRNA against survivin can block survivin expression in PC-2 and MCF-7 cells efficiently and specifically. Down regulation of survivin expression can suppress proliferation of PC-2 and MCF-7 cells. Survivin RNAi may have potential value in gene therapy of human cancers.</p>
Subject(s)
Female , Humans , Base Sequence , Breast Neoplasms , Pathology , Therapeutics , Cell Line, Tumor , Cell Proliferation , Gene Expression , Inhibitor of Apoptosis Proteins , Microtubule-Associated Proteins , Genetics , Metabolism , Pancreatic Neoplasms , Pathology , Therapeutics , Plasmids , Genetics , RNA, Messenger , Genetics , Metabolism , RNA, Neoplasm , Genetics , Metabolism , RNA, Small Interfering , Genetics , Therapeutic Uses , TransfectionABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of a sequence-specific small interfering RNA (siRNA) in suppressing survivin expression and cell proliferation and inducing apoptosis of PC-2 cells.</p><p><b>METHODS</b>The plasmid expression vector of siRNA targeted against survivin was constructed and transfected into PC-2 cells with Lipofectamine 2000. The changes of survivin expression were detected by semi-quantitative RT-PCR and immunohistochemical SP methods. The effect of siRNA in suppressing the proliferation of PC-2 cells was detected by MTT assay, and its role in inducing PC-2 cell apoptosis evaluated by flow cytometry.</p><p><b>RESULTS</b>The sequence-specific siRNA effectively suppressed survivin expression at both mRNA and protein levels with inhibition rate of 81.25% at mRNA level and 74.24% at protein level. Survivin expression suppression significantly inhibited the proliferation of PC-2 cells, and at 24 and 48 h after cell seeding, the proliferation inhibition rate was 28.00% and 33.38% respectively; 24, 48 h after the transfection, apoptosis occurred in 8.46% and 7.53% of the cells, respectively.</p><p><b>CONCLUSIONS</b>The plasmid expression vector for the siRNA against survivin constructed in the study can effectively and specifically suppress survivin expression in PC-2 cells, and blocking survivin expression suppresses PC-2 cell proliferation and induces cell apoptosis. siRNA targeted against survivin has a potential value in gene therapy for pancreatic cancer.</p>
Subject(s)
Humans , Apoptosis , Genetics , Cell Line, Tumor , Cell Proliferation , Cell Survival , Genetics , Inhibitor of Apoptosis Proteins , Microtubule-Associated Proteins , Genetics , Neoplasm Proteins , Genetics , Pancreatic Neoplasms , Genetics , Pathology , RNA Interference , RNA, Messenger , Genetics , RNA, Small Interfering , Genetics , TransfectionABSTRACT
<p><b>OBJECTIVE</b>Blocking the expression of survivin with RNA interference techniques, the effects of suppressing proliferation and inducing apoptosis of breast cancer MCF-7 cells were investigated.</p><p><b>METHODS</b>A siRNA eukaryotic expression vector against survivin was constructed and transfected into breast cancer MCF-7 cells with lipofectamine 2000. The changes of survivin expression were detected by semi-quantitive RT-PCR and immunohistochemistry. The effect of suppressing proliferation of MCF-7 cell was detected by MTT assay. The effect of inducing MCF-7 cell apoptosis was detected by TUNEL assay.</p><p><b>RESULTS</b>The sequence-specific siRNA can efficiently block the expression of survivin both at mRNA and protein levels. The expression inhibition rate was 64.9% at mRNA level detected by semi-quantitive RT-PCR and 79.7% at protein level detected by immunohistochemistry. Blocking the expression of survivin can suppress proliferation of MCF-7 cells significantly. At 24 and 48 h after the cells were reseeded, the proliferation inhibition rates were 31.6% and 33.0%, respectively. At 24 h after transfection, apoptosis was induced in 12.9% of the cells as detected by TUNEL assay.</p><p><b>CONCLUSION</b>Blocking the expression of survivin with RNA interference technology can significantly suppress proliferation of MCF-7 cells and induce apoptosis to a certain degree. RNAi targeted to survivin has a potential value in gene therapy of breast cancer.</p>