1. Resources
  2. Citations Library

Headers act as filters

  • Records
      1. Author :
        Georgel, P.; Radosavljevic, M.; Macquin, C.; Bahram, S.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Mol Immunol
      6. Products :
      7. Volume :
        48
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Xen14, Xen 14, E. coli Xen14, IVIS, Animals; Cell Line, Tumor; Female; Histocompatibility Antigens Class I/genetics/*immunology; Humans; Klebsiella Infections/*immunology/prevention & control; Klebsiella pneumoniae/*immunology; Male; Mice; Mice, Inbred C57BL; Mice, Knockout
      12. Abstract :
        As opposed to the well established role of MHC-linked, polymorphic, class I (MHC-I) genes in adaptive immunity, a universal role for non-conventional MHC-I is unknown, thus requiring a case-by-case study. The MHC unlinked, monomorphic, but beta(2)microglobulin (beta(2)m)-associated “MHC class I related” MR1 molecule interacts with a semi-invariant TCR. The pathophysiology of this interaction or more importantly of this peculiar MHC-I remains mostly unknown. Recently it was shown that beta(2)m deficient mice were more susceptible to infection by Klebsiella pneumoniae, a widely spread Gram-negative bacteria that causes diverse and often severe ailments in man. Here we demonstrate, using both an in vivo imaging system and survival tests, the increased susceptibility to K. pneumoniae (but not to several other Gram negative bacteria) of MR1 deficient mice. This is accompanied by a consequent change in body temperature and systemic cytokine profile. Hence MR1 controls K. pneumoniae infection in vivo.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21190736
      14. Call Number :
        PKI @ kd.modi @ 9
      15. Serial :
        10392
      1. Author :
        Tsurumi, C.; Esser, N.; Firat, E.; Gaedicke, S.; Follo, M.; Behe, M.; Elsasser-Beile, U.; Grosu, A. L.; Graeser, R.; Niedermann, G.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        PLoS One
      6. Products :
      7. Volume :
        5
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IntegriSense, Animals; Antigens, CD/*biosynthesis/*metabolism; Flow Cytometry/methods; Glioma/metabolism; Glycoproteins/*biosynthesis/*metabolism; Humans; Hybridomas/metabolism; Mice; Mice, Transgenic; Models, Biological; Neoplasm Metastasis; Neoplasm Transplantation; Neoplasms/*metabolism; Neoplastic Stem Cells; Peptides/*metabolism; Recurrence
      12. Abstract :
        BACKGROUND: Cancer stem cells are thought to play a pivotal role in tumor maintenance, metastasis, tumor therapy resistance and relapse. Hence, the development of methods for non-invasive in vivo detection of cancer stem cells is of great importance. METHODOLOGY/PRINCIPAL FINDINGS: Here, we describe successful in vivo detection of CD133/prominin, a cancer stem cell surface marker for a variety of tumor entities. The CD133-specific monoclonal antibody AC133.1 was used for quantitative fluorescence-based optical imaging of mouse xenograft models based on isogenic pairs of CD133 positive and negative cell lines. A first set consisted of wild-type U251 glioblastoma cells, which do not express CD133, and lentivirally transduced CD133-overexpressing U251 cells. A second set made use of HCT116 colon carcinoma cells, which uniformly express CD133 at levels comparable to primary glioblastoma stem cells, and a CD133-negative HCT116 derivative. Not surprisingly, visualization and quantification of CD133 in overexpressing U251 xenografts was successful; more importantly, however, significant differences were also found in matched HCT116 xenograft pairs, despite the lower CD133 expression levels. The binding of i.v.-injected AC133.1 antibodies to CD133 positive, but not negative, tumor cells isolated from xenografts was confirmed by flow cytometry. CONCLUSIONS/SIGNIFICANCE: Taken together, our results show that non-invasive antibody-based in vivo imaging of tumor-associated CD133 is feasible and that CD133 antibody-based tumor targeting is efficient. This should facilitate developing clinically applicable cancer stem cell imaging methods and CD133 antibody-based therapeutics.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21187924
      14. Call Number :
        PKI @ kd.modi @ 15
      15. Serial :
        10382
      1. Author :
        Goldberg, M.S.; Xing, D.; Ren, Y.; Orsulic, S.; Bhatia, S.N.; Sharp, P.A.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Proceedings of the National Academy of Sciences of the United States of America
      6. Products :
      7. Volume :
        108
      8. Issue :
        2
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        brca1; Cancer; In vivo imaging (VisEn); IVIS Spectrum imaging system; mice; siRNA; vivotag-750
      12. Abstract :
        Inhibition of the DNA repair enzyme poly(ADP-ribose) polymerase 1 (PARP1) with small molecules has been shown to be an effective treatment for ovarian cancer with BRCA mutations. Here, we report the in vivo administration of siRNA to Parp1 in mouse models of ovarian cancer. A unique member of the lipid-like materials known as lipidoids is shown to deliver siRNA to disseminated murine ovarian carcinoma allograft tumors following intraperitoneal (i.p.) injection. siParp1 inhibits cell growth, primarily by induction of apoptosis, in Brca1-deficient cells both in vitro and in vivo. Additionally, the treatment extends the survival of mice bearing tumors derived from Brca1-deficient ovarian cancer cells but not from Brca1 wild-type cells, confirming the proposed mechanism of synthetic lethality. Because there are 17 members of the Parp family, the inherent complementarity of RNA affords a high level of specificity for therapeutically addressing Parp1 in the context of impaired homologous recombination.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21187397
      14. Call Number :
        PKI @ user @ 8448
      15. Serial :
        4805
      1. Author :
        Goldberg, M. S.; Xing, D.; Ren, Y.; Orsulic, S.; Bhatia, S. N.; Sharp, P. A.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Proc Natl Acad Sci U S A
      6. Products :
      7. Volume :
        108
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        VivoTag, IVIS, Vivotag, Animals; BRCA1 Protein/*genetics; Drug Carriers; Drug Delivery Systems; Female; Humans; Mice; Nanoparticles/*chemistry; Nanotechnology/methods; Neoplasm Transplantation; Ovarian Neoplasms/*genetics/*therapy; Poly(ADP-ribose) Polymerases/*genetics; RNA Interference; RNA, Small Interfering/*metabolism; Treatment Outcome
      12. Abstract :
        Inhibition of the DNA repair enzyme poly(ADP-ribose) polymerase 1 (PARP1) with small molecules has been shown to be an effective treatment for ovarian cancer with BRCA mutations. Here, we report the in vivo administration of siRNA to Parp1 in mouse models of ovarian cancer. A unique member of the lipid-like materials known as lipidoids is shown to deliver siRNA to disseminated murine ovarian carcinoma allograft tumors following intraperitoneal (i.p.) injection. siParp1 inhibits cell growth, primarily by induction of apoptosis, in Brca1-deficient cells both in vitro and in vivo. Additionally, the treatment extends the survival of mice bearing tumors derived from Brca1-deficient ovarian cancer cells but not from Brca1 wild-type cells, confirming the proposed mechanism of synthetic lethality. Because there are 17 members of the Parp family, the inherent complementarity of RNA affords a high level of specificity for therapeutically addressing Parp1 in the context of impaired homologous recombination.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21187397
      14. Call Number :
        PKI @ kd.modi @ 5
      15. Serial :
        10566
      1. Author :
        Emmett, M. S.; Lanati, S.; Dunn, D. B.; Stone, O. A.; Bates, D. O.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Microcirculation
      6. Products :
      7. Volume :
        18
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS, B16-F10-luc-G5, B16F10-luc-G5, B16-F10-luc, B16F10-luc,
      12. Abstract :
        OBJECTIVE: To determine whether chemotactic-metastasis, the preferential growth of melanomas towards areas of high lymphatic density, is CCL21/CCR7 dependent in vivo. Lymphatic endothelial cells (LECs) produce the chemokine CCL21. Metastatic melanoma cells express CCR7, its receptor, and exhibit chemotactic-metastasis, whereby metastatic cells recognise and grow towards areas of higher lymphatic density. METHODS: We used two in vivo models of directional growth towards depots of LECs of melanoma cells over-expressing CCR7. Injected LEC were tracked by intravital fluorescence microscopy, and melanoma growth by bioluminescence. RESULTS: Over-expression of the chemokine receptor CCR7 enables non-metastatic tumor cells to recognise and grow towards LECs (3.9 fold compared with control), but not blood endothelial cells (0.9 fold), in vitro and in vivo in the absence of increased lymphatic clearance. Chemotactic metastasis was inhibited by a CCL21 neutralising antibody (4-17% of control). Furthermore, CCR7 expression in mouse B16 melanomas resulted in in-transit metastasis (50-100% of mice) that was less often seen with control tumors (0-50%) in vivo. CONCLUSION: These results suggest that recognition of LEC by tumors expressing receptors for lymphatic specific ligands contributes towards the identification and invasion of lymphatics by melanoma cells and provides further evidence for a chemotactic metastasis model of tumor spread.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21166932
      14. Call Number :
        PKI @ kd.modi @ 2
      15. Serial :
        10355
      1. Author :
        Mathew, B.; Lennon, F.E.; Siegler, J.; Mirzapoiazova, T.; Mambetsariev, N.; Sammani, S.; Gerhold, L.M.; Lariviere, P.J.; Chen, C.-T.; Garcia, J.G.N.; Salgia, R.; Moss, J.; Singleton, P.A.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Anesthesia and Analgesia
      6. Products :
      7. Volume :
        112
      8. Issue :
        3
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Cancer; flank tumor; In vivo; MMPSense 750; ProSense 680; tomography; VisEn FMT
      12. Abstract :
        <AbstractText Label=“BACKGROUND” NlmCategory=“BACKGROUND”>The possibility that μ opioid agonists can influence cancer recurrence is a subject of recent interest. Epidemiologic studies suggested that there were differences in cancer recurrence in breast and prostate cancer contingent on anesthetic regimens. In this study, we identify a possible mechanism for these epidemiologic findings on the basis of μ opioid receptor (MOR) regulation of Lewis lung carcinoma (LLC) tumorigenicity in cell and animal models.</AbstractText> <AbstractText Label=“METHODS” NlmCategory=“METHODS”>We used human lung tissue and human non-small cell lung cancer (NSCLC) cell lines and evaluated MOR expression using immunoblot and immunohistochemical analysis. LLC cells were treated with the peripheral opioid antagonist methylnaltrexone (MNTX) or MOR shRNA and evaluated for proliferation, invasion, and soft agar colony formation in vitro and primary tumor growth and lung metastasis in C57BL/6 and MOR knockout mice using VisEn fluorescence mediated tomography imaging and immunohistochemical analysis.</AbstractText> <AbstractText Label=“RESULTS” NlmCategory=“RESULTS”>We provide several lines of evidence that the MOR may be a potential target for lung cancer, a disease with high mortality and few treatment options. We first observed that there is ~5- to 10-fold increase in MOR expression in lung samples from patients with NSCLC and in several human NSCLC cell lines. The MOR agonists morphine and [d-Ala(2), N-MePhe(4), Gly-ol]-enkephalin (DAMGO) increased in vitro LLC cell growth. Treatment with MNTX or silencing MOR expression inhibited LLC invasion and anchorage-independent growth by 50%-80%. Injection of MOR silenced LLC lead to a ~65% reduction in mouse lung metastasis. In addition, MOR knockout mice do not develop significant tumors when injected with LLC in comparison with wild-type controls. Finally, continuous infusion of the peripheral opioid antagonist MNTX attenuates primary LLC tumor growth and reduces lung metastasis.</AbstractText> <AbstractText Label=“CONCLUSIONS” NlmCategory=“CONCLUSIONS”>Taken together, our data suggest a possible direct effect of opiates on lung cancer progression, and provide a plausible explanation for the epidemiologic findings. Our observations further suggest a possible therapeutic role for opioid antagonists.</AbstractText>
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21156980
      14. Call Number :
        PKI @ user @ 8557
      15. Serial :
        4797
      1. Author :
        Liu, W. F.; Ma, M.; Bratlie, K. M.; Dang, T. T.; Langer, R.; Anderson, D. G.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2011
      5. Publication :
        Biomaterials
      6. Products :
      7. Volume :
        32
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        ProSense, IVIS, Animals; Biocompatible Materials/*adverse effects; Cells, Cultured; Free Radicals/metabolism; Immunohistochemistry; Male; Mice; Prostheses and Implants/*adverse effects; Reactive Oxygen Species/*metabolism
      12. Abstract :
        The non-specific host response to implanted biomaterials is often a key challenge of medical device design. To evaluate biocompatibility, measuring the release of reactive oxygen species (ROS) produced by inflammatory cells in response to biomaterial surfaces is a well-established method. However, the detection of ROS in response to materials implanted in vivo has not yet been demonstrated. Here, we develop a bioluminescence whole animal imaging approach to observe ROS released in response to subcutaneously-implanted materials in live animals. We compared the real-time generation of ROS in response to two representative materials, polystyrene and alginate, over the course of 28 days. High levels of ROS were observed near polystyrene, but not alginate implants, and persisted throughout the course of 28 days. Histological analysis revealed that high levels of ROS correlated not only with the presence of phagocytic cells at early timepoints, but also fibrosis at later timepoints, suggesting that ROS may be involved in both the acute and chronic phase of the foreign body response. These data are the first in vivo demonstration of ROS generation in response to implanted materials, and describe a novel technique to evaluate the host response.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21146868
      14. Call Number :
        PKI @ kd.modi @ 3
      15. Serial :
        10428
      1. Author :
        Lu, Z.; Dai, T.; Huang, L.; Kurup, D. B.; Tegos, G. P.; Jahnke, A.; Wharton, T.; Hamblin, M. R.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Nanomedicine (Lond)
      6. Products :
      7. Volume :
        5
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Xen5, Xen 5, Pseudomonas aeruginosa Xen 5, Animals; Fullerenes/*chemistry; Male; Mice; Mice, Inbred BALB C; Photochemotherapy/*methods; Photosensitizing Agents/*chemistry; Pseudomonas Infections/*drug therapy; Pseudomonas aeruginosa/drug effects; Wound Infection/*drug therapy
      12. Abstract :
        AIMS: Fullerenes are under intensive study for potential biomedical applications. We have previously reported that a C60 fullerene functionalized with three dimethylpyrrolidinium groups (BF6) is a highly active broad-spectrum antimicrobial photosensitizer in vitro when combined with white-light illumination. We asked whether this high degree of in vitro activity would translate into an in vivo therapeutic effect in two potentially lethal mouse models of infected wounds. MATERIALS & METHODS: We used stable bioluminescent bacteria and a low light imaging system to follow the progress of the infection noninvasively in real time. An excisional wound on the mouse back was contaminated with one of two bioluminescent Gram-negative species, Proteus mirabilis (2.5 x 10(7) cells) and Pseudomonas aeruginosa (5 x 10(6) cells). A solution of BF6 was placed into the wound followed by delivery of up to 180 J/cm(2) of broadband white light (400-700 nm). RESULTS: In both cases there was a light-dose-dependent reduction of bioluminescence from the wound not observed in control groups (light alone or BF6 alone). Fullerene-mediated photodynamic therapy of mice infected with P. mirabilis led to 82% survival compared with 8% survival without treatment (p < 0.001). Photodynamic therapy of mice infected with highly virulent P. aeruginosa did not lead to survival, but when photodynamic therapy was combined with a suboptimal dose of the antibiotic tobramycin (6 mg/kg for 1 day) there was a synergistic therapeutic effect with a survival of 60% compared with a survival of 20% with tobramycin alone (p < 0.01). CONCLUSION: These data suggest that cationic fullerenes have clinical potential as an antimicrobial photosensitizer for superficial infections where red light is not needed to penetrate tissue.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21143031
      14. Call Number :
        PKI @ kd.modi @ 2
      15. Serial :
        10390