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      1. Author :
        Stangenberg L, Ellson C, Cortez-Retamozo V, Ortiz-Lopez A, Yuan H, Blois J, Smith RA, Yaffe MB, Weissleder R, Benoist C, Mathis D, Josephson L and Mahmood U
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2009
      5. Publication :
        Arthritis and Rheumatism
      6. Products :
      7. Volume :
        60
      8. Issue :
        8
      9. Page Numbers :
        N/A
      10. Research Area :
        Physiology
      11. Keywords :
        ProSense; AngioSense; arthritis; in vivo imaging
      12. Abstract :
        OBJECTIVE: To test a novel self-activating viridin (SAV) prodrug that slowly releases wortmannin, a potent phosphoinositide 3-kinase inhibitor, in a model of antibody-mediated inflammatory arthritis.

        METHODS: The SAV prodrug was administered to K/BxN mice or to C57BL/6 (B6) mice that had been injected with K/BxN serum. Ankle thickness was measured, and histologic changes were scored after a 10-day disease course (serum-transfer arthritis). Protease activity was measured by a near-infrared imaging approach using a cleavable cathepsin-selective probe. Further near-infrared imaging techniques were used to analyze early changes in vascular permeability after serum injection, as well as neutrophil-endothelial cell interactions. Neutrophil functions were assessed using an oxidative burst assay as well as a degranulation assay.

        RESULTS: SAV prevented ankle swelling in mice with serum-transfer arthritis in a dose-dependent manner. It also markedly reduced the extent of other features of arthritis, such as protease activity and histology scores for inflammation and joint erosion. Moreover, SAV was an effective therapeutic agent. The underlying mechanisms for the antiinflammatory activity were manifold. Endothelial permeability after serum injection was reduced, as was firm neutrophil attachment to endothelial cells. Endothelial cell activation by tumor necrosis factor alpha was impeded by SAV, as measured by the expression of vascular cell adhesion molecule. Crucial neutrophil functions, such as generation of reactive oxygen species and degranulation of protease-laden vesicles, were decreased by SAV administration.

        CONCLUSION: A novel SAV prodrug proved strongly antiinflammatory in a murine model of antibody-induced inflammatory arthritis. Its activity could be attributed, at least in part, to the inhibition of neutrophil and endothelial cell functions.
      13. URL :
        http://onlinelibrary.wiley.com/doi/10.1002/art.24704/abstract
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4528
      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 :
        Dernell, William S.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2005
      5. Publication :
        N/A
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        *Breast Cancer; *Chemotherapy; *Genes; *Luciferase; Anatomy and Physiology; Biochemistry; Bioware; Cells(Biology); Diseases; Drugs; Efficacy; Gel Polymers; Gels; Growth(Physiology); Humans; Image Processing; In Vitro Analysis.; In Vivo Analysis; Luciferase Genes; Medicine and Medical Research; Metastasis; Mouse Models; Paclitaxel Sensitivity; Poloxamer Polymers; Polymers; Preclinical Evaluations; surgery; Synergism; Toxicity; Tumor Cell Lines
      12. Abstract :
        This project evaluated paclitaxel chemotherapy delivery from a gel polymer system placed into a wound bed following conservative (marginal) surgical removal of human breast cancers grown in nude mice. This delivery method was shown to control local tumor disease as well as assist in control of systemic metastasis. We established 5 human breast cancer cell lines within our laboratory. We elected purchase and implement a unique (luciferase) imaging system which allows in vivo imaging of tumor growth and metastasis (and subsequently decrease animal use). Tumor cell lines were transfected with the luciferase gene. In vitro testing of cell lines established paclitaxel sensitivity and showed a synergistic effect of delivering paclitaxel by the poloxamer polymer, especially for the chemotherapy resistant cell line, MCF-7-ADR. We completed the simultaneous evaluation of local and systemic toxicity, local, regional and systemic distribution and local and systemic efficacy of locally delivered paclitaxel chemotherapy following tumor removal using the MCF-7-ADR cell line in nude mice. Intracavitary administration of taxol in poloxamer was well tolerated (locally and systemically) afld resulted in significantly improved control of local tumor regrowth and comparable control of metastasis following marginal tumor removal as compared to intravenous paclitaxel (parent drug) . Sustained drug levels (from polymer delivery) were seen in plasma and liver tissue at 60 days.
      13. URL :
        http://oai.dtic.mil/oai/oai?verb=getRecord&metadataPrefix=html&identifier=ADA437225
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8994
      1. Author :
        Steve H. Thorne; Yoram Barak; Wenchuan Liang; Michael H. Bachmann; Jianghong Rao; Christopher H. Contag; A. Matin
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2009
      5. Publication :
        Molecular Cancer Therapeutics
      6. Products :
      7. Volume :
        8
      8. Issue :
        2
      9. Page Numbers :
        N/A
      10. Research Area :
        Cancer
      11. Keywords :
        Cancer; in vivo imaging; drug discovery; chemotherapy
      12. Abstract :
        We report the discovery of a new prodrug, 6-chloro-9-nitro-5-oxo-5H-benzo(a)phenoxazine (CNOB). This prodrug is efficiently activated by ChrR6, the highly active prodrug activating bacterial enzyme we have previously developed. The CNOB/ChrR6 therapy was effective in killing several cancer cell lines in vitro. It also efficiently treated tumors in mice with up to 40% complete remission. 9-Amino-6-chloro-5H-benzo(a)phenoxazine-5-one (MCHB) was the only product of CNOB reduction by ChrR6. MCHB binds DNA; at nonlethal concentration, it causes cell accumulation in the S phase, and at lethal dose, it induces cell surface Annexin V and caspase-3 and caspase-9 activities. Further, MCHB colocalizes with mitochondria and disrupts their electrochemical potential. Thus, killing by CNOB involves MCHB, which likely induces apoptosis through the mitochondrial pathway. An attractive feature of the CNOB/ChrR6 regimen is that its toxic product, MCHB, is fluorescent. This feature proved helpful in in vitro studies because simple fluorescence measurements provided information on the kinetics of CNOB activation within the cells, MCHB killing mechanism, its generally efficient bystander effect in cells and cell spheroids, and its biodistribution. The emission wavelength of MCHB also permitted its visualization in live animals, allowing noninvasive qualitative imaging of MCHB in mice and the tumor microenvironment. This feature may simplify exploration of barriers to the penetration of MCHB in tumors and their amelioration.
      13. URL :
        http://mct.aacrjournals.org/content/8/2/333.abstract
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4500
      1. Author :
        Galina Gabriely, Thomas Wurdinger, Santosh Kesari, Christine C. Esau, Julja Burchard, Peter S. Linsley and Anna M. Krichevsky
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2008
      5. Publication :
        Molecular and Cellular Biology
      6. Products :
      7. Volume :
        28
      8. Issue :
        17
      9. Page Numbers :
        N/A
      10. Research Area :
        Neuroscience
      11. Keywords :
        in vivo imaging; MMPSense; microRNA 21; glioma
      12. Abstract :
        Substantial data indicate that microRNA 21 (miR-21) is significantly elevated in glioblastoma (GBM) and in many other tumors of various origins. This microRNA has been implicated in various aspects of carcinogenesis, including cellular proliferation, apoptosis, and migration. We demonstrate that miR-21 regulates multiple genes associated with glioma cell apoptosis, migration, and invasiveness, including the RECK and TIMP3 genes, which are suppressors of malignancy and inhibitors of matrix metalloproteinases (MMPs). Specific inhibition of miR-21 with antisense oligonucleotides leads to elevated levels of RECK and TIMP3 and therefore reduces MMP activities in vitro and in a human model of gliomas in nude mice. Moreover, downregulation of miR-21 in glioma cells leads to decreases of their migratory and invasion abilities. Our data suggest that miR-21 contributes to glioma malignancy by downregulation of MMP inhibitors, which leads to activation of MMPs, thus promoting invasiveness of cancer cells. Our results also indicate that inhibition of a single oncomir, like miR-21, with specific antisense molecules can provide a novel therapeutic approach for “physiological” modulation of multiple proteins whose expression is deregulated in cancer.
      13. URL :
        http://mcb.asm.org/cgi/content/abstract/28/17/5369
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4546
      1. Author :
        Min, Jung-Joon; Nguyen, Vu H.; Gambhir, Sanjiv S.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Nuclear Medicine and Molecular Imaging
      6. Products :
      7. Volume :
        44
      8. Issue :
        1
      9. Page Numbers :
        15-24
      10. Research Area :
        N/A
      11. Keywords :
        Cancer; Cardiology; Gene delivery vector; Gene Therapy; Imaging / Radiology; Molecular Imaging; Nuclear Medicine; Oncology; Orthopedics; Xen26
      12. Abstract :
        Cancer persists as one of the most devastating diseases in the world. Problems including metastasis and tumor resistance to chemotherapy and radiotherapy have seriously limited the therapeutic effects of present clinical treatments. To overcome these limitations, cancer gene therapy has been developed over the last two decades for a broad spectrum of applications, from gene replacement and knockdown to vaccination, each with different requirements for gene delivery. So far, a number of genes and delivery vectors have been investigated, and significant progress has been made with several gene therapy modalities in clinical trials. Viral vectors and synthetic liposomes have emerged as the vehicles of choice for many applications. However, both have limitations and risks that restrict gene therapy applications, including the complexity of production, limited packaging capacity, and unfavorable immunological features. While continuing to improve these vectors, it is important to investigate other options, particularly nonviral biological agents such as bacteria, bacteriophages, and bacteria-like particles. Recently, many molecular imaging techniques for safe, repeated, and high-resolution in vivo imaging of gene expression have been employed to assess vector-mediated gene expression in living subjects. In this review, molecular imaging techniques for monitoring biological gene delivery vehicles are described, and the specific use of these methods at different steps is illustrated. Linking molecular imaging to gene therapy will eventually help to develop novel gene delivery vehicles for preclinical study and support the development of future human applications.
      13. URL :
        http://link.springer.com/article/10.1007/s13139-009-0006-3
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        10003
      1. Author :
        Houari Korideck; Jeffrey D. Peterson
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2009
      5. Publication :
        Journal of Pharmacology and Experimental Therapeutics
      6. Products :
      7. Volume :
        329
      8. Issue :
        3
      9. Page Numbers :
        N/A
      10. Research Area :
        Cardiovascular Research; Biology
      11. Keywords :
        in vivo imaging; therapeutics; asthma; pulmonary diseases; noninvasive; infrared imaging; fluorescence molecular tomography; FMT; Fluorescence Imaging Agents
      12. Abstract :
        Animal models of pulmonary inflammation are critical for understanding the pathophysiology of asthma and for developing new therapies. Current conventional assessments in mouse models of asthma and chronic obstructive pulmonary disease rely on invasive measures of pulmonary function and terminal characterization of cells infiltrating into the lung. The ability to noninvasively visualize and quantify the underlying biological processes in mouse pulmonary models in vivo would provide a significant advance in characterizing disease processes and the effects of therapeutics. We report the utility of near-infrared imaging agents, in combination with fluorescence molecular tomography (FMT) imaging, for the noninvasive quantitative imaging of mouse lung inflammation in an ovalbumin (OVA)-induced chronic asthma model. BALB/c mice were intraperitoneally sensitized with OVA-Alum (aluminum hydroxide) at days 0 and 14, followed by daily intranasal challenge with OVA in phosphate-buffered saline from days 21 to 24. Dexamethasone and control therapies were given intraperitoneally 4 h before each intranasal inhalation of OVA from days 21 to 24. Twenty-four hours before imaging, the mice were injected intravenously with 5 nmol of the cathepsin-activatable fluorescent agent, ProSense 680. Quantification by FMT revealed in vivo cysteine protease activity within the lung associated with the inflammatory eosinophilia, which decreased in response to dexamethasone treatment. Results were correlated with in vitro laboratory tests (bronchoalveolar lavage cell analysis and immunohistochemistry) and revealed good correlation between these measures and quantification of ProSense 680 activation. We have demonstrated the ability of FMT to noninvasively visualize and quantify inflammation in the lung and monitor therapeutic efficacy in vivo.
      13. URL :
        http://jpet.aspetjournals.org/content/329/3/882.full
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4473
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