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      1. Author :
        N/A
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2007
      5. Publication :
        Lasers in surgery and medicine
      6. Products :
      7. Volume :
        39
      8. Issue :
        1
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Anti-Infective Agents; Biofilms; Dental Pulp Cavity; Dental Pulp Diseases; Endodontics; Humans; Luminescence; Photochemotherapy; Polyethyleneimine; Porphyrins; Proteus Infections; Proteus mirabilis; Pseudomonas aeruginosa; Pseudomonas Infections; Xen5; Xen44
      12. Abstract :
        BACKGROUND AND OBJECTIVE To compare the effectiveness of antimicrobial photodynamic therapy (PDT), standard endodontic treatment and the combined treatment to eliminate bacterial biofilms present in infected root canals. STUDY DESIGN/MATERIALS AND METHODS Ten single-rooted freshly extracted human teeth were inoculated with stable bioluminescent Gram-negative bacteria, Proteus mirabilis and Pseudomonas aeruginosa to form 3-day biofilms in prepared root canals. Bioluminescence imaging was used to serially quantify bacterial burdens. PDT employed a conjugate between polyethylenimine and chlorin(e6) as the photosensitizer (PS) and 660-nm diode laser light delivered into the root canal via a 200-micro fiber, and this was compared and combined with standard endodontic treatment using mechanical debridement and antiseptic irrigation. RESULTS Endodontic therapy alone reduced bacterial bioluminescence by 90% while PDT alone reduced bioluminescence by 95%. The combination reduced bioluminescence by >98%, and importantly the bacterial regrowth observed 24 hours after treatment was much less for the combination (P<0.0005) than for either single treatment. CONCLUSIONS Bioluminescence imaging is an efficient way to monitor endodontic therapy. Antimicrobial PDT may have a role to play in optimized endodontic therapy.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/17066481
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        9997
      1. Author :
        De Kwaadsteniet, Michele
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2009
      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 :
        Antibiotics -- Therapeutic use; Bacteriocins; Bioware; Dissertations -- Microbiology; Drug resistance in microorganisms; Nisin; Respiratory infections -- Treatment; Skin -- Infections -- Treatment; Staphylococcus aureus; Theses -- Microbiology; Xen29
      12. Abstract :
        Multidrug resistant strains of Staphylococcus aureus is presenting an increasing threat, especially immune compromised individuals. Many of these strains have developed resistance to newly approved drugs such as quinupristin-dalfopristin, linezolid and daptomycin. The search for alternative treatment, including bacteriocins (ribosomally synthesized antimicrobial peptides) of lactic acid bacteria is increasing . Lactococcus lactis subsp. lactis F10, isolated from freshwater catfish, produced a new nisin variant active against clinical strains of S. aureus. The operon encoding nisin F is located on a plasmid and the structural gene has been sequenced. The lantibiotic is closely related to nisin Z, except at position 30 where valine replaced isoleucine. The antimicrobial activity of nisin F against S. aureus was tested in the respiratory tract of Wistar rats. Non-immunosuppressed and immunosuppressed rats were intranasally infected with S. aureus K and then treated with either nisin F or sterile physiological saline. Nisin F protected immunosuppressed rats against S. aureus, as symptoms of an infection were only detected in the trachea and lungs of immunosuppressed rats treated with saline. The safety of intranasally administered nisin F was also evaluated and proved to have no adverse side effects. The potential of nisin F as an antimicrobial agent to treat subcutaneous skin infections was evaluated by infecting C57BL/6 mice with a bioluminescent strain of S. aureus (Xen 36). Immunosuppressed mice were treated with either nisin F or sterile physiological saline 24 h and 48 h after infection with subcutaneously injected S. aureus Xen 36. Histology and bioluminescence flux measurements revealed that nisin F was ineffective in the treatment of deep dermal staphylococcal infections. Non-infected and infected mice treated with nisin F had an influx of polymorphonuclear cells in the deep stroma of the skin tissue. This suggested that nisin F, when injected subcutaneously, may have modulated the immune system. Nisin F proved an effective antimicrobial agent against S. aureus-related infections in the respiratory tract, but not against subcutaneous infections. The outcome of nisin F treatment thus depends on the route of administration and site of infection.
      13. URL :
        http://scholar.sun.ac.za/handle/10019.1/1285
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        9042
      1. Author :
        N/A
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2009
      5. Publication :
        PloS one
      6. Products :
      7. Volume :
        4
      8. Issue :
        3
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Antineoplastic Agents; Bioware; Breast Neoplasms; Cell Line, Tumor; Cell Movement; Cell Proliferation; Cell Survival; Diphosphonates; Esterification; Female; Humans; Hydrophobic and Hydrophilic Interactions; MDA-MB-231-D3H2LN cells; Neoplasm Metastasis; Structure-Activity Relationship
      12. Abstract :
        BACKGROUND Although there was growing evidence in the potential use of Bisphosphonates (BPs) in cancer therapy, their strong osseous affinities that contrast their poor soft tissue uptake limited their use. Here, we developed a new strategy to overcome BPs hydrophilicity by masking the phosphonic acid through organic protecting groups and introducing hydrophobic functions in the side chain. METHODOLOGY/PRINCIPAL FINDINGS We synthesized non-nitrogen BPs (non N-BPs) containing bromobenzyl group (BP7033Br) in their side chain that were symmetrically esterified with hydrophobic 4-methoxphenyl (BP7033BrALK) and assessed their effects on breast cancer estrogen-responsive cells (T47D, MCF-7) as well as on non responsive ones (SKBR3, MDA-MB-231 and its highly metastatic derived D3H2LN subclone). BP7033Br ALK was more efficient in inhibiting tumor cell proliferation, migration and survival when compared to BP7033Br. Although both compounds inhibited tumor growth without side effects, only BP7033Br ALK abrogated tumor angiogenesis and D3H2LN cells-induced metastases formation. CONCLUSION/SIGNIFICANCE Taken together these data suggest the potential therapeutic use of this new class of esterified Bisphosphonates (BPs) in the treatment of tumor progression and metastasis without toxic adverse effects.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/19262688
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8958
      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 and Rheumatism
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Apo866; Arthritis; In vivo; Living Image software; MMPSense 750 FAST; Xenogen Caliper IVIS 200
      12. Abstract :
        OBJECTIVE: Using APO866, studies assessed the ability of Pre-B-cell colony-Enhancing Factor (PBEF) to regulate inflammatory and degradative processes in fibroblasts and collagen-induced arthritis. METHODS: ELISAs were used to examine regulation of metalloproteinases and chemokine expression by HFF fibroblasts. PBEF was further examined in the collagen-induced arthritis model using APO866. Disease activity was assessed using radiography, histology, in vivo imaging and quantitative PCR (qPCR). RESULTS: In vitro activation of fibroblasts with PBEF promoted MMP-3, CCL-2 and CXCL-8 expression, an effect inhibited by APO866. Early intervention with APO866 in collagen-induced arthritis inhibited both synovial inflammation, including chemokine-directed leukocyte infiltration, and the systemic marker of inflammation, serum hyaluronic acid. Blockade of degenerative processes by APO866 was further illustrated by the reduced expression of MMP-3 and MMP-13 in joint extracts and reduction of the systemic marker of cartilage erosion, serum cartilage oligomeric matrix protein (COMP). Radiology showed that APO866 protected against bone erosion, whilst qPCR demonstrated inhibition of RANKL expression. APO866 treatment in established disease (clinical score >=5) reduced synovial inflammation, cartilage destruction and halted bone erosion. MMP-3, CCL-2 and RANKL activity, as assessed by in vivo imaging with MMPSense750 and qPCR were reduced in treated animals. qPCR of synovial explants from animals with CIA showed that APO866 inhibited MMP-3, CCL-2 and RANKL production, a result that was reversed with nicotinamide mononucleotide (NMN) CONCLUSIONS: These data confirm PBEF to be an important regulator of inflammation, cartilage catabolism and bone erosion, and highlights APO866 as a promising therapy for targeting PBEF activity in inflammatory arthritis.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/21400478
      14. Call Number :
        PKI @ user @ 8551
      15. Serial :
        4800
      1. Author :
        Kristof Schutters and Chris Reutelingsperger
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2010
      5. Publication :
        Apoptosis
      6. Products :
      7. Volume :
        15
      8. Issue :
        9
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Apoptosis; Phosphatidylserine; Annexin A5; Molecular Imaging; Targeted Drug Delivery; in vivo imaging; FMT; fluorescence molecular tomography; Annexin-Vivo
      12. Abstract :
        Cells are able to execute apoptosis by activating series of specific biochemical reactions. One of the most prominent characteristics of cell death is the externalization of phosphatidylserine (PS), which in healthy cells resides predominantly in the inner leaflet of the plasma membrane. These features have made PS-externalization a well-explored phenomenon to image cell death for diagnostic purposes. In addition, it was demonstrated that under certain conditions viable cells express PS at their surface such as endothelial cells of tumor blood vessels, stressed tumor cells and hypoxic cardiomyocytes. Hence, PS has become a potential target for therapeutic strategies aiming at Targeted Drug Delivery. In this review we highlight the biomarker PS and various PS-binding compounds that have been employed to target PS for diagnostic purposes. We emphasize the 35 kD human protein annexin A5, that has been developed as a Molecular Imaging agent to measure cell death in vitro, and non-invasively in vivo in animal models and in patients with cardiovascular diseases and cancer. Recently focus has shifted from diagnostic towards therapeutic applications employing annexin A5 in strategies to deliver drugs to cells that express PS at their surface.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2929432/?tool=pubmed
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4562
      1. Author :
        Filip K. Swirski, Ralph Weissleder and Mikael J. Pittet
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        N/A
      5. Publication :
        Arteriosclerosis, Thrombosis, and Vascular Biology
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        Cardiovascular Research
      11. Keywords :
        atherosclerosis; in vivo imaging; monocytes; VivoTag; FMT; fluorescence molecular tomography
      12. Abstract :
        Monocytes and macrophages play active roles in atherosclerosis, a chronic inflammatory disease that is a leading cause of death in the developed world. The prevailing paradigm states that, during human atherogenesis, monocytes accumulate in the arterial intima and differentiate into macrophages, which then ingest oxidized lipoproteins, secrete a diverse array of proinflammatory mediators, and eventually become foam cells, the key constituents of a vulnerable plaque. Yet monocytes are heterogeneous. In the mouse, one subset (Ly-6Chi) promotes inflammation, expands in hypercholesterolemic conditions, and selectively gives rise to macrophages in atheromata. A different subset (Ly-6Clo) attenuates inflammation and promotes angiogenesis and granulation tissue formation in models of tissue injury, but its role in atherosclerosis is largely unknown. In the human, monocyte heterogeneity is preserved but it is still unresolved how subsets correspond functionally. The contradistinctive properties of these cells suggest commitment for specific function before infiltrating tissue. Such commitment argues for discriminate targeting of deleterious subsets while sparing host defense and repair mechanisms. In addition to advancing our understanding of atherosclerosis, the ability to target and image monocyte subsets would allow us to evaluate drugs designed to selectively inhibit monocyte subset recruitment or function, and to stratify patients at risk for developing complications such as myocardial infarction or stroke. In this review we summarize recent advances of our understanding of the behavioral heterogeneity of monocytes during disease progression and outline emerging molecular imaging approaches to address key questions in the field.
      13. URL :
        http://atvb.ahajournals.org/cgi/content/abstract/ATVBAHA.108.180521v1
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4569
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