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      1. Author :
        Kosaka, N.; Iguchi, H.; Yoshioka, Y.; Hagiwara, K.; Takeshita, F.; Ochiya, T.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        J Biol Chem
      6. Products :
      7. Volume :
        287
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        PC-3M-luc-C6, PC-3M-luc, IVIS, Bioware, Prostate cancer, Bioluminescence
      12. Abstract :
        Normal epithelial cells regulate the secretion of autocrine and paracrine factors that prevent aberrant growth of neighboring cells, leading to healthy development and normal metabolism. One reason for tumor initiation is considered to be a failure of this homeostatic cell competitive system. Here we identify tumor-suppressive microRNAs (miRNAs) secreted by normal cells as anti-proliferative signal entities. Culture supernatant of normal epithelial prostate PNT-2 cells attenuated proliferation of PC-3M-luc cells, prostate cancer cells. Global analysis of miRNA expression signature revealed that a variety of tumor-suppressive miRNAs are released from PNT-2 cells. Of these miRNAs, secretory miR-143 could induce growth inhibition exclusively in cancer cells in vitro and in vivo. These results suggest that secretory tumor-suppressive miRNAs can act as a death signal in a cell competitive process. This study provides a novel insight into a tumor initiation mechanism.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22123823
      14. Call Number :
        PKI @ kd.modi @ 2
      15. Serial :
        10537
      1. Author :
        M van Eekelen; LS Sasportas; R Kasmieh; S Yip; J-L Figueiredo; DN Louis; R Weissleder; K Shah
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Oncogene
      6. Products :
      7. Volume :
        29
      8. Issue :
        22
      9. Page Numbers :
        N/A
      10. Research Area :
        Cancer
      11. Keywords :
        brain tumor; glioma; human neural stem cells; TSP-1; endothelial cells; angiogenesis; in vivo imaging
      12. Abstract :
        Novel therapeutic agents combined with innovative modes of delivery and non-invasive imaging of drug delivery, pharmacokinetics and efficacy are crucial in developing effective clinical anticancer therapies. In this study, we have created and characterized multiple novel variants of anti-angiogenic protein thrombospondin (aaTSP-1) that comprises unique regions of three type-I-repeats of TSP-1 and used engineered human neural stem cells (hNSC) to provide sustained on-site delivery of secretable aaTSP-1 to tumor-vasculature. We show that hNSC-aaTSP-1 has anti-angiogenic effect on human brain and dermal microvascular endothelial cells co-cultured with established glioma cells and CD133+ glioma-initiating cells. Using human glioma cells and hNSC engineered with different combinations of fluorescent and bioluminescent marker proteins and employing multi-modality imaging techniques, we show that aaTSP-1 targets the vascular-component of gliomas and a single administration of hNSC-aaTSP-1 markedly reduces tumor vessel-density that results in inhibition of tumor-progression and increased survival in mice bearing highly malignant human gliomas. We also show that therapeutic hNSC do not proliferate and remain in an un-differentiated state in the brains of glioma-bearing mice. This study provides a platform for accelerated development of future cell-based therapies for cancer.
      13. URL :
        http://www.nature.com/onc/journal/v29/n22/abs/onc201075a.html
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4492
      1. Author :
        Figg, William D; Li, Haiqing; Sissung, Tristan; Retter, Avi; Wu, Shenhong; Gulley, James L; Arlen, Phil; Wright, John J; Parnes, Howard; Fedenko, Kathy; Latham, Lea; Steinberg, Seth M; Jones, Elizabeth; Chen, Clara; Dahut, William
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2007
      5. Publication :
        BJU international
      6. Products :
      7. Volume :
        99
      8. Issue :
        5
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Aged; Androgens; Animals; Antineoplastic Combined Chemotherapy Protocols; Aryl Hydrocarbon Hydroxylases; Bioware; Cytochrome P-450 Enzyme System; Estramustine; Genotype; Humans; Male; Mice; Mice, Nude; Middle Aged; PC-3M-luc; Prostatic Neoplasms; Survival Analysis; Taxoids; Thalidomide; Treatment Outcome
      12. Abstract :
        OBJECTIVE To evaluate the combination of docetaxel plus estramustine (which prolongs survival in patients with androgen-independent prostate cancer, AIPC), and thalidomide (that also adds to docetaxel activity), both pre-clinically and clinically in AIPC. PATIENTS, MATERIALS AND METHODS In the pre-clinical evaluation we injected PC3 cells subcutaneously into severely combined immunodeficient mice and started treatment after the tumour volume reached 50 mm3. We also evaluated the combination using luciferase-labelled PC3M-luc-C6 cells in nude mice. We enrolled 20 patients with metastatic progressive AIPC into a phase II clinical trial to evaluate this combination. Docetaxel (30 mg/m2) was administered every week, for 3 of 4 weeks. The dose of thalidomide was 200 mg/day and estramustine was given three times a day at 1, 2, 3, 8, 9, 10, 15, 16 and 17 days. RESULTS In the mice, thalidomide with docetaxel plus estramustine reduced tumour volume by 88% at 17 days vs the control treatment (p=0.001). The combination of docetaxel, estramustine and thalidomide nearly eradicated the signal from the luciferase-expressing PC3M cells in the metastasis model. Clinically, the progression-free time was 7.2 months with this combination; 18 of 20 patients had a decline of half or more in prostate-specific antigen level and two of 10 patients with soft-tissue lesions had a partial response on computed tomography. There were 24 grade 3 and two grade 4 complications associated with this combination. There was a statistically significant association between overall survival and the CYP1B1*3 genotype (P=0.013). CONCLUSION Docetaxel-based chemotherapy is now regarded as a standard regimen for metastatic AIPC. The combination of estramustine, docetaxel and thalidomide is an advantageous treatment in pre-clinical models of prostate cancer and is a safe, tolerable and active regimen in patients with AIPC.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/17437439
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8970
      1. Author :
        Engelsman, Anton F; van Dam, Gooitzen M; van der Mei, Henny C; Busscher, Henk J; Ploeg, Rutger J
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Annals of surgery
      6. Products :
      7. Volume :
        251
      8. Issue :
        1
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Abdominal Wall; Animals; Bioware; Female; Luminescent Measurements; Mice; Mice, Inbred BALB C; Polypropylenes; Polytetrafluoroethylene; pXen-5; Staphylococcal Infections; Staphylococcus aureus; Surgical Mesh; Xen29
      12. Abstract :
        OBJECTIVE To study the influence of morphology of surgical meshes on the course of bacterial infection under the influence of the host immune system in an in vivo chronic bacterial infection model. BACKGROUND The use of prosthetic meshes has increased dramatically the last decades in abdominal wall reconstructive surgery. Whereas infection is becoming a more frequent complication, attention is increasingly drawn to the influence of the surgeon's mesh choice on the course of this complication. METHODS Samples of 6 often applied surgical meshes were contaminated with a bioluminescent strain of Staphylococcus aureus and implanted subcutaneously in an immunocompetent BALB/c mouse. The intensity and the spreading of bioluminescence (ie, p/s/cm/sr) were analyzed non-invasively in vivo during a 10-day follow-up period. RESULTS Over the course of infection, multifilament polypropylene and hydrophobic materials showed a significantly higher persistence of bacteria as well as spreading of infection compared to all other meshes. In contrast, infection resolved in almost all animals with a low-weight polyester mesh. CONCLUSION The results of this study are in accordance with circumstantial evidence from limited clinical reports on infection involving surgical meshes and suggest that multifilament and hydrophobic meshes significantly increase bacterial persistence or spreading in the infected area in contrast to monofilament polypropylene and lightweight meshes. Therefore, the surgeon should consider this outcome when choosing a mesh graft for limiting infection in abdominal wall repair.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/19864938
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        9017
      1. Author :
        Matthias Nahrendorf, Peter Waterman, Greg Thurber, Kevin Groves, Milind Rajopadhye, Peter Panizzi, Brett Marinelli, Elena Aikawa, Mikael J Pittet, Filip K Swirski and Ralph Weissleder
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2009
      5. Publication :
        Arteriosclerosis, Thrombosis, and Vascular Biology
      6. Products :
      7. Volume :
        29
      8. Issue :
        10
      9. Page Numbers :
        N/A
      10. Research Area :
        Cardiovascular Research
      11. Keywords :
        FMT-CT; molecular imaging; atherosclerosis; protease activity; inflammation; in vivo imaging; fluorescence molecular tomography; ProSense
      12. Abstract :
        Objective: Proteases are emerging biomarkers of inflammatory diseases. In atherosclerosis, these enzymes are often secreted by inflammatory macrophages, digest the extracellular matrix of the fibrous cap and destabilize atheromata. Protease function can be monitored with protease activatable imaging probes and quantitated in vivo by fluorescence molecular tomography (FMT). To address two major constraints currently associated with imaging of murine atherosclerosis (lack of highly sensitive probes and absence of anatomical information), we compared protease sensors (PS) of variable size and pharmacokinetics and co-registered FMT datasets with computed tomography (FMT-CT).

        Methods and results: Co-registration of FMT and CT was achieved with a multimodal imaging cartridge containing fiducial markers detectable by both modalities. A high-resolution CT angiography protocol accurately localized fluorescence to the aortic root of atherosclerotic apoE-/- mice. To identify suitable sensors, we first modeled signal kinetics in-silico and then compared three probes with identical oligo-L-lysine cleavage sequences: PS-5, 5nm in diameter containing 2 fluorochromes , PS-25, a 25nm version with an elongated lysine chain and PS-40, a polymeric nanoparticle. Serial FMT-CT showed fastest kinetics for PS-5 but, surprisingly, highest fluorescence in lesions of the aortic root for PS-40. PS-40 robustly reported therapeutic effects of atorvastatin, corroborated by ex vivo imaging and qPCR for the model protease cathepsin B.

        Conclusions: FMT-CT is a robust and observer-independent tool for non-invasive assessment of inflammatory murine atherosclerosis. Reporter-containing nanomaterials may have unique advantages over small molecule agents for in vivo imaging.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746251/?tool=pubmed
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4568
      1. Author :
        Krespi, Y. P.; Kizhner, V.; Nistico, L.; Hall-Stoodley, L.; Stoodley, P.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Am J Otolaryngol
      6. Products :
      7. Volume :
        32
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Xen31, Xen 31, MRSA, S. aureus, IVIS, Bioluminescence, Biofilms/drug effects/*radiation effects; Ciprofloxacin/*pharmacology; Culture Media; High-Energy Shock Waves; Humans; *Laser Therapy, Low-Level; Methicillin-Resistant Staphylococcus aureus/*growth &; development/physiology/*radiation effects; Microbial Sensitivity Tests; Reference Values; Sensitivity and Specificity; Spectroscopy, Near-Infrared; Staphylococcal Infections/drug therapy
      12. Abstract :
        OBJECTIVE: The aim of the study was to study the efficacy of 2 different lasers in vitro, in disrupting biofilm and killing planktonic pathogenic bacteria. MATERIALS AND METHODS: Biofilms of a stable bioluminescent of Staphylococcus aureus Xen 31 were grown in a 96-well microtiter plate for 3 days. The study included 7 arms: (a) control; (b) ciprofloxacin (3 mg/L, the established minimum inhibitory concentration [MIC]) alone; (c) shock wave (SW) laser alone; (d) near-infrared (NIR) laser alone; (e) SW laser and ciprofloxacin; (f) SW and NIR lasers; (g) SW, NIR lasers, and ciprofloxacin. The results were evaluated with an in vivo imaging system (IVIS) biophotonic system (for live bacteria) and optical density (OD) for total bacteria. RESULTS: Without antibiotics, there was a 43% reduction in OD (P < .05) caused by the combination of SW and NIR suggesting that biofilm had been disrupted. There was an 88% reduction (P < .05) in live biofilm. Ciprofloxacin alone resulted in a decrease of 28% of total live cells (biofilm remaining attached) and 58% of biofilm cells (both P > .05). Ciprofloxacin in combination with SW and SW + NIR lasers caused a decrease of more than 60% in total live biomass and more than 80% of biofilm cells, which was significantly greater than ciprofloxacin alone (P < .05). CONCLUSIONS: We have demonstrated an effective nonpharmacologic treatment method for methicillin-resistant Staphylococcus aureus (MRSA) biofilm disruption and killing using 2 different lasers. The preferred treatment sequence is a SW laser disruption of biofilm followed by NIR laser illumination. Treatment optimization of biofilm is possible with the addition of ciprofloxacin in concentrations consistent with planktonic MIC.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/20434806
      14. Call Number :
        PKI @ kd.modi @ 2
      15. Serial :
        10554
      1. Author :
        Derwall, M.; Malhotra, R.; Lai, C. S.; Beppu, Y.; Aikawa, E.; Seehra, J. S.; Zapol, W. M.; Bloch, K. D.; Yu, P. B.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Arterioscler Thromb Vasc Biol
      6. Products :
      7. Volume :
        32
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        OsteoSense, Animals; Anti-Inflammatory Agents/pharmacology; Antioxidants/pharmacology; Atherosclerosis/etiology/genetics/metabolism/pathology/*prevention & control; Bone Morphogenetic Protein Receptors, Type I/metabolism; Bone Morphogenetic Proteins/*antagonists & inhibitors/metabolism; Cardiovascular Agents/*pharmacology; Cholesterol, LDL/blood; Diet, High-Fat; Disease Models, Animal; Endothelial Cells/drug effects/metabolism; Fatty Liver/etiology/metabolism/prevention & control; Female; Hep G2 Cells; Humans; Lipoproteins, LDL/metabolism; Liver/drug effects/metabolism; Mice; Mice, Inbred C57BL; Mice, Knockout; Pyrazoles/*pharmacology; Pyrimidines/*pharmacology; Reactive Oxygen Species/metabolism; Receptors, LDL/deficiency/genetics; Recombinant Fusion Proteins/metabolism; Signal Transduction/*drug effects; Time Factors; Vascular Calcification/etiology/genetics/metabolism/pathology/*prevention &; control
      12. Abstract :
        OBJECTIVE: The expression of bone morphogenetic proteins (BMPs) is enhanced in human atherosclerotic and calcific vascular lesions. Although genetic gain- and loss-of-function experiments in mice have supported a causal role of BMP signaling in atherosclerosis and vascular calcification, it remains uncertain whether BMP signaling might be targeted pharmacologically to ameliorate both of these processes. METHODS AND RESULTS: We tested the impact of pharmacological BMP inhibition on atherosclerosis and calcification in LDL receptor-deficient (LDLR-/-) mice. LDLR-/- mice fed a high-fat diet developed abundant vascular calcification within 20 weeks. Prolonged treatment of LDLR-/- mice with the small molecule BMP inhibitor LDN-193189 was well-tolerated and potently inhibited development of atheroma, as well as associated vascular inflammation, osteogenic activity, and calcification. Administration of recombinant BMP antagonist ALK3-Fc replicated the antiatherosclerotic and anti-inflammatory effects of LDN-193189. Treatment of human aortic endothelial cells with LDN-193189 or ALK3-Fc abrogated the production of reactive oxygen species induced by oxidized LDL, a known early event in atherogenesis. Unexpectedly, treatment of mice with LDN-193189 lowered LDL serum cholesterol by 35% and markedly decreased hepatosteatosis without inhibiting HMG-CoA reductase activity. Treatment with BMP2 increased, whereas LDN-193189 or ALK3-Fc inhibited apolipoprotein B100 secretion in HepG2 cells, suggesting that BMP signaling contributes to the regulation of cholesterol biosynthesis. CONCLUSION: These results definitively implicate BMP signaling in atherosclerosis and calcification, while uncovering a previously unidentified role for BMP signaling in LDL cholesterol metabolism. BMP inhibition may be helpful in the treatment of atherosclerosis and associated vascular calcification.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22223731
      14. Call Number :
        PKI @ kd.modi @ 5
      15. Serial :
        10469
      1. Author :
        Elena S. Izmailova; Nancy Paz; Herlen Alencar; Miyoung Chun; Lisa Schopf; Michael Hepperle; Joan H. Lane; Geraldine Harriman; Yajun Xu; Timothy Ocain; Ralph Weissleder; Umar Mahmood; Aileen M. Healy; Bruce Jaffee
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2007
      5. Publication :
        Arthritis and Rheumatism
      6. Products :
      7. Volume :
        56
      8. Issue :
        1
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        inflammation; immune response; rheumatoid arthritis; arthritis; in vivo imaging
      12. Abstract :
        OBJECTIVE: The NF-kappaB signaling pathway promotes the immune response in rheumatoid arthritis (RA) and in rodent models of RA. NF-kappaB activity is regulated by the IKK-2 kinase during inflammatory responses. To elucidate how IKK-2 inhibition suppresses disease development, we used a combination of in vivo imaging, transcription profiling, and histopathology technologies to study mice with antibody-induced arthritis.

        METHODS: ML120B, a potent, small molecule inhibitor of IKK-2, was administered to arthritic animals, and disease activity was monitored. NF-kappaB activity in diseased joints was quantified by in vivo imaging. Quantitative reverse transcriptase-polymerase chain reaction was used to evaluate gene expression in joints. Protease-activated near-infrared fluorescence (NIRF) in vivo imaging was applied to assess the amounts of active proteases in the joints.

        RESULTS: Oral administration of ML120B suppressed both clinical and histopathologic manifestations of disease. In vivo imaging demonstrated that NF-kappaB activity in inflamed arthritic paws was inhibited by ML120B, resulting in significant suppression of multiple genes in the NF-kappaB pathway, i.e., KC, epithelial neutrophil-activating peptide 78, JE, intercellular adhesion molecule 1, CD3, CD68, tumor necrosis factor alpha, interleukin-1beta, interleukin-6, inducible nitric oxide synthase, cyclooxygenase 2, matrix metalloproteinase 3, cathepsin B, and cathepsin K. NIRF in vivo imaging demonstrated that ML120B treatment dramatically reduced the amount of active proteases in the joints.

        CONCLUSION: Our data demonstrate that IKK-2 inhibition in the murine model of antibody-induced arthritis suppresses both inflammation and joint destruction. In addition, this study highlights how gene expression profiling can facilitate the identification of surrogate biomarkers of disease activity and treatment response in an experimental model of arthritis.
      13. URL :
        http://onlinelibrary.wiley.com/doi/10.1002/art.22303/abstract
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4511
      1. Author :
        Evans, L.; Williams, A. S.; Hayes, A. J.; Jones, S. A.; Nowell, M.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Arthritis Rheum
      6. Products :
      7. Volume :
        63
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        MMPSense, IVIS, Acrylamides/pharmacology/*therapeutic use; Animals; Arthritis, Experimental/*drug therapy/metabolism/pathology; Cartilage/*metabolism/pathology; Fibroblasts/metabolism/pathology; Humans; Inflammation/metabolism/pathology; Leukocytes/*drug effects/metabolism/pathology; Mice; Nicotinamide Phosphoribosyltransferase/*antagonists & inhibitors; Piperidines/pharmacology/*therapeutic use
      12. Abstract :
        OBJECTIVE: To assess the ability of pre-B cell colony-enhancing factor (PBEF) to regulate inflammation and degradative processes in inflammatory arthritis, using the small molecule inhibitor APO866 in human fibroblasts in vitro and in murine collagen-induced arthritis (CIA). METHODS: Enzyme-linked immunosorbent assays were used to examine regulation of expression of metalloproteinases and chemokines in human fibroblasts. The role of PBEF was further examined using APO866 in mice with CIA, with effects on disease activity assessed using radiography, histology, in vivo imaging, and quantitative polymerase chain reaction (qPCR). RESULTS: In vitro activation of human fibroblasts with PBEF promoted expression of matrix metalloproteinase 3 (MMP-3), CCL2, and CXCL8, an effect inhibited by APO866. In mice with CIA, early intervention with APO866 inhibited synovial inflammation, including chemokine-directed leukocyte infiltration, and reduced a systemic marker of inflammation, serum hyaluronic acid. APO866 blockade led to reduced expression of MMP-3 and MMP-13 in joint extracts and to a reduction in a systemic marker of cartilage erosion, serum cartilage oligomeric matrix protein. Radiologic images revealed that APO866 protected against bone erosion, while qPCR demonstrated inhibition of RANKL expression. In mice with established disease, APO866 reduced synovial inflammation and cartilage destruction, and halted bone erosion. In addition, APO866 reduced the activity of MMP-3, CCL2, and RANKL in vivo, and inhibited production of CCL2 and RANKL in synovial explants from arthritic mice, a result that was reversed with nicotinamide mononucleotide. CONCLUSION: These findings confirm PBEF to be an important regulator of inflammation, cartilage catabolism, and bone erosion, and highlight APO866 as a promising therapeutic agent for targeting PBEF activity in inflammatory arthritis.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21400478
      14. Call Number :
        PKI @ kd.modi @ 2
      15. Serial :
        10460
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