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      1. Author :
        N/A
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2007
      5. Publication :
        Brazilian dental journal
      6. Products :
      7. Volume :
        18
      8. Issue :
        3
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Colony Count, Microbial; Cuspid; Dental Pulp Cavity; Disinfectants; Drug Combinations; Genetic Engineering; Humans; Hydrogen peroxide; Incisor; Luminescent Measurements; Luminescent Proteins; Maxilla; Pseudomonas aeruginosa; Root Canal Irrigants; Root Canal Preparation; Sensitivity and Specificity; Sodium Hypochlorite; Xen5
      12. Abstract :
        Microbial infection plays an important role in the development of pulp necrosis and formation of periapical lesions. In vitro and in vivo research in this field, traditionally microbiological culture methods using paper point sampling and quantitative culture, faces difficulties in completely removing bacteria from the root canal system and analyzing sequential procedures. This study employed genetically engineered bioluminescent bacteria and a light-sensitive imaging system to allow real-time visualization of the infection. Ten extracted teeth incubated with P. aeruginosa were treated by mechanical instrumentation with K-files (#30 K-file, #35 K-file and #40 K-file) and chemical irrigation with sodium hypochlorite and hydrogen peroxide. Irrigation alone reduced the contamination in 18%; the first chemomechanical sequence (instrumentation with a #30 K-file + irrigation) provided 41% of reduction; the second sequence (#35 K-file + irrigation) achieved 62%; and the complete therapy (#30 K-file + #35 K-file + #40 K-file + irrigation) achieved 93% of bacterial reduction. These results suggest that the endodontic treatment is dependent on the association of a chemical and mechanical approaches and that root canal enlargement improves bacterial reduction probably because the irrigation has more access to the apical third.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/18176710
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        9998
      1. Author :
        Kozlowski, C.; Weimer, R. M.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        PLoS One
      6. Products :
      7. Volume :
        7
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        AngioSense, Animals; Antigens, CD/metabolism; Antigens, Differentiation, Myelomonocytic/metabolism; Calcium-Binding Proteins/metabolism; Central Nervous System/metabolism; Green Fluorescent Proteins/genetics/*metabolism; Immunohistochemistry/*methods; Lipopolysaccharides/pharmacology; Mice; Mice, Inbred C57BL; Mice, Transgenic; Microfilament Proteins/metabolism; Microglia/cytology/drug effects/*metabolism; Microscopy, Confocal/*methods; Receptors, Cytokine/genetics/metabolism; Receptors, HIV/genetics/metabolism; Reproducibility of Results
      12. Abstract :
        Microglia are specialized immune cells of the brain. Upon insult, microglia initiate a cascade of cellular responses including a characteristic change in cell morphology. To study the dynamics of microglia immune response in situ, we developed an automated image analysis method that enables the quantitative assessment of microglia activation state within tissue based solely on cell morphology. Per cell morphometric analysis of fluorescently labeled microglia is achieved through local iterative threshold segmentation, which reduces errors caused by signal-to-noise variation across large volumes. We demonstrate, utilizing systemic application of lipopolysaccharide as a model of immune challenge, that several morphological parameters, including cell perimeter length, cell roundness and soma size, quantitatively distinguish resting versus activated populations of microglia within tissue comparable to traditional immunohistochemistry methods. Furthermore, we provide proof-of-concept data that monitoring soma size enables the longitudinal assessment of microglia activation in the mouse neocortex imaged via 2-photon in vivo microscopy. The ability to quantify microglia activation automatically by shape alone allows unbiased and rapid analysis of both fixed and in vivo central nervous system tissue.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22457705
      14. Call Number :
        PKI @ kd.modi @ 8
      15. Serial :
        10435
      1. Author :
        Chen, J.; Gallo, K. A.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        Cancer Res
      6. Products :
      7. Volume :
        72
      8. Issue :
        N/A
      9. Page Numbers :
        4130-40
      10. Research Area :
        N/A
      11. Keywords :
        MDA-MB-231-luc2-tdtomato, IVIS, tdtomato, fluorescent protein, Animals; Breast Neoplasms/enzymology/*metabolism/*pathology; Cell Line, Tumor; Cell Movement/*physiology; Chemokine CXCL12/metabolism; Female; Humans; MAP Kinase Kinase Kinases/*metabolism; MAP Kinase Signaling System; Mice; Mice, Nude; Neoplasm Invasiveness; Paxillin/*metabolism; Phosphorylation
      12. Abstract :
        MLK3 kinase activates multiple mitogen-activated protein kinases and plays a critical role in cancer cell migration and invasion. In the tumor microenvironment, prometastatic factors drive breast cancer invasion and metastasis, but their associated signaling pathways are not well-known. Here, we provide evidence that MLK3 is required for chemokine (CXCL12)-induced invasion of basal breast cancer cells. We found that MLK3 induced robust phosphorylation of the focal adhesion scaffold paxillin on Ser 178 and Tyr 118, which was blocked by silencing or inhibition of MLK3-JNK. Silencing or inhibition of MLK3, inhibition of JNK, or expression of paxillin S178A all led to enhanced Rho activity, indicating that the MLK3-JNK-paxillin axis limits Rho activity to promote focal adhesion turnover and migration. Consistent with this, MLK3 silencing increased focal adhesions and stress fibers in breast cancer cells. MLK3 silencing also decreased the formation of breast cancer lung metastases in vivo, and breast cancer cells derived from mouse lung metastases showed enhanced Ser 178 paxillin phosphorylation. Taken together, our findings suggest that the MLK3-JNK-paxillin signaling axis may represent a potential therapeutic target and/or prognostic marker in breast cancer metastasis.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22700880
      14. Call Number :
        PKI @ kd.modi @ 1
      15. Serial :
        10495
      1. Author :
        David E Sosnovik, Matthias Nahrendorf and Ralph Weissleder
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2008
      5. Publication :
        Nature Reviews Cardiology
      6. Products :
      7. Volume :
        5
      8. Issue :
        2
      9. Page Numbers :
        N/A
      10. Research Area :
        Cardiovascular Research
      11. Keywords :
        in vivo imaging; fluorescence imaging, molecular imaging, MRI, myocardium, SPECT; MMPSense
      12. Abstract :
        Molecular imaging agents can be targeted to a specific receptor or protein on the cardiomyocyte surface, or to enzymes released into the interstitial space, such as cathepsins, matrix metalloproteinases and myeloperoxidase. Molecular imaging of the myocardium, however, requires the imaging agent to be small, sensitive (nanomolar levels or better), and able to gain access to the interstitial space. Several novel agents that fulfill these criteria have been used for targeted molecular imaging applications in the myocardium. Magnetic resonance, fluorescence, and single-photon emission CT have been used to image the molecular signals generated by these agents. The use of targeted imaging agents in the myocardium has the potential to provide valuable insights into the pathophysiology of myocardial injury and to facilitate the development of novel therapeutic strategies.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597275/?tool=pubmed
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4650
      1. Author :
        Sadikot, R. T.; Blackwell, T. S.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2008
      5. Publication :
        Methods Mol Biol
      6. Products :
      7. Volume :
        477
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Adenoviridae/genetics, Anesthesia, Animals, Firefly Luciferin/administration & dosage/pharmacology, *Gene Expression Regulation/drug effects, Genetic Vectors/genetics, Luciferases/metabolism, Luminescent Measurements/*methods, Mice, Photons, Whole Body Imaging/*methods IVIS, Xenogen, Xen5
      12. Abstract :
        Molecular imaging offers many unique opportunities to study biological processes in intact organisms. Bioluminescence is the emission of light from biochemical reactions that occur within a living organism. Luciferase has been used as a reporter gene in transgenic mice but, until bioluminescence imaging was described, the detection of luciferase activity required either sectioning of the animal or excision of tissue and homogenization to measure enzyme activities in a conventional luminometer. Bioluminescence imaging (BLI) is based on the idea that biological light sources can be incorporated into cells and animal models artificially that does not naturally express the luminescent genes. This imaging modality has proven to be a very powerful methodology to detect luciferase reporter activity in intact animal models. This form of optical imaging is low cost and noninvasive and facilitates real-time analysis of disease processes at the molecular level in living organisms. Bioluminescence provides a noninvasive method to monitor gene expression in vivo and has enormous potential to elucidate the pathobiology of lung diseases in intact mouse models, including models of inflammation/injury, infection, and cancer.
      13. URL :
        http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=19082962
      14. Call Number :
        142705
      15. Serial :
        5558
      1. Author :
        Leuschner, F.; Rauch, P. J.; Ueno, T.; Gorbatov, R.; Marinelli, B.; Lee, W. W.; Dutta, P.; Wei, Y.; Robbins, C.; Iwamoto, Y.; Sena, B.; Chudnovskiy, A.; Panizzi, P.; Keliher, E.; Higgins, J. M.; Libby, P.; Moskowitz, M. A.; Pittet, M. J.; Swirski, F. K.; Weissleder, R.; Nahrendorf, M.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        J Exp Med
      6. Products :
      7. Volume :
        209
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IntegriSense, Adoptive Transfer; Animals; Biological Markers/metabolism; Cell Death/genetics; Disease Models, Animal; Female; *Hematopoiesis, Extramedullary; Inflammation/immunology/metabolism; Interleukin-1beta/genetics/metabolism; Kinetics; Macrophages/cytology/*physiology; Mice; Mice, Inbred C57BL; Mice, Knockout; Models, Biological; Monocytes/*cytology/*physiology; Myeloid Cells/metabolism; Myocardial Infarction/immunology/pathology/*physiopathology; Signal Transduction; Spleen/physiology; Stroke/immunology/metabolism; Wound Healing/physiology
      12. Abstract :
        Monocytes (Mo) and macrophages (MPhi) are emerging therapeutic targets in malignant, cardiovascular, and autoimmune disorders. Targeting of Mo/MPhi and their effector functions without compromising innate immunity's critical defense mechanisms first requires addressing gaps in knowledge about the life cycle of these cells. Here we studied the source, tissue kinetics, and clearance of Mo/MPhi in murine myocardial infarction, a model of acute inflammation after ischemic injury. We found that a) Mo tissue residence time was surprisingly short (20 h); b) Mo recruitment rates were consistently high even days after initiation of inflammation; c) the sustained need of newly made Mo was fostered by extramedullary monocytopoiesis in the spleen; d) splenic monocytopoiesis was regulated by IL-1beta; and e) the balance of cell recruitment and local death shifted during resolution of inflammation. Depending on the experimental approach, we measured a 24 h Mo/MPhi exit rate from infarct tissue between 5 and 13% of the tissue cell population. Exited cells were most numerous in the blood, liver, and spleen. Abrogation of extramedullary monocytopoiesis proved deleterious for infarct healing and accelerated the evolution of heart failure. We also detected rapid Mo kinetics in mice with stroke. These findings expand our knowledge of Mo/MPhi flux in acute inflammation and provide the groundwork for novel anti-inflammatory strategies for treating heart failure.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22213805
      14. Call Number :
        PKI @ kd.modi @ 27
      15. Serial :
        10370
      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
      1. Author :
        Penn-Barwell, J. G.; Murray, C. K.; Wenke, J. C.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        J Bone Joint Surg Br
      6. Products :
      7. Volume :
        94
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Xen36, Xen 36, Staphylococcus aureus Xen36, IVIS
      12. Abstract :
        Most animal studies indicate that early irrigation and debridement reduce infection after an open fracture. Unfortunately, these studies often do not involve antibiotics. Clinical studies indicate that the timing of initial debridement does not affect the rate of infection but these studies are observational and fraught with confounding variables. The purpose of this study was to control these variables using an animal model incorporating systemic antibiotics and surgical treatment. We used a rat femur model with a defect which was contaminated with Staphylococcus aureus and treated with a three-day course of systemic cefazolin (5 mg/kg 12-hourly) and debridement and irrigation, both of which were initiated independently at two, six and 24 hour time points. After 14 days the bone and hardware were harvested for separate microbiological analysis. No animal that received antibiotics and surgery two hours after injury had detectable bacteria. When antibiotics were started at two hours, a delay in surgical treatment from two to six hours significantly increased the development of infection (p = 0.047). However, delaying surgery to 24 hours increase the rate of infection, but not significantly (p = 0.054). The timing of antibiotics had a more significant effect on the proportion of positive samples than earlier surgery. Delaying antibiotics to six or 24 hours had a profoundly detrimental effect on the infection rate regardless of the timing of surgery. These findings are consistent with the concept that bacteria progress from a vulnerable planktonic form to a treatment-resistant biofilm.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/22219257
      14. Call Number :
        PKI @ kd.modi @ 10
      15. Serial :
        10404
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