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      1. Author :
        Woelfle, Mark A; Xu, Yao; Qin, Ximing; Johnson, Carl Hirschie
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2007
      5. Publication :
        Proceedings of the National Academy of Sciences of the United States of America
      6. Products :
      7. Volume :
        104
      8. Issue :
        47
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Bioware; Circadian Rhythm; Cyanobacteria; DNA, Bacterial; DNA, Superhelical; Gene Expression Regulation, Bacterial; Light; Plasmids; Promoter Regions, Genetic; pXen-13; Transcription, Genetic
      12. Abstract :
        The cyanobacterium Synechococcus elongatus expresses robust circadian (daily) rhythms under the control of the KaiABC-based core clockwork. Unlike eukaryotic circadian systems characterized thus far, the cyanobacterial clockwork modulates gene expression patterns globally and specific clock gene promoters are not necessary in mediating the circadian feedback loop. The oscilloid model postulates that global rhythms of transcription are based on rhythmic changes in the status of the cyanobacterial chromosome that are ultimately controlled by the KaiABC oscillator. By using a nonessential, cryptic plasmid (pANS) as a reporter of the superhelical state of DNA in cyanobacteria, we show that the supercoiling status of this plasmid changes in a circadian manner in vivo. The rhythm of topological change in the plasmid is conditional; this change is rhythmic in constant light and in light/dark cycles, but not in constant darkness. In further support of the oscilloid model, cyanobacterial promoters that are removed from their native chromosomal locations and placed on a plasmid preserve their circadian expression patterns.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/18000054
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        9031
      1. Author :
        Wunder A and Klohs J.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2008
      5. Publication :
        Basic Research in Cardiology
      6. Products :
      7. Volume :
        103
      8. Issue :
        2
      9. Page Numbers :
        N/A
      10. Research Area :
        Cardiovascular Research
      11. Keywords :
        In vivo imaging; atherosclerosis; bioluminescence imaging; fluorescence imaging; myocardial infarction; stroke; ProSense
      12. Abstract :
        Pathophysiological processes in the vascular system are the major cause of mortality and disease. Atherosclerosis, an inflammatory process in arterial walls, can lead to formation of plaques, whose rupture can lead to thrombus formation, obstruction of vessels (thrombosis), reduction of the blood flow (ischemia), cell death in the tissue fed by the occluded vessel, and depending on the affected vessel, to myocardial infarction or stroke. Imaging techniques enabling visualization of the biological processes involved in this scenario are therefore highly desirable. In recent years, a number of reporter agents and reporter systems have been developed to visualize these processes using different imaging modalities including nuclear imaging techniques, such as positron emission tomography or single photon emission computed tomography, magnetic resonance imaging, and ultrasound. This article comprises a brief overview of optical imaging techniques, such as fluorescence imaging and bioluminescence imaging for the visualization of vascular pathophysiology.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/18324374
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4649
      1. Author :
        Jan Grimm; David G. Kirsch; Stephen D. Windsor; Carla F. Bender Kim; Philip M. Santiago; Vasilis Ntziachristos; Tyler Jacks; Ralph Weissleder
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2005
      5. Publication :
        PNAS
      6. Products :
      7. Volume :
        102
      8. Issue :
        40
      9. Page Numbers :
        N/A
      10. Research Area :
        Cancer
      11. Keywords :
        gene expression profiling; lung cancer; immunohistochemistry; Western blotting; in vivo imaging; moleuclar imaging; fluorescence molecular tomography
      12. Abstract :
        Using gene expression profiling, we identified cathepsin cysteine proteases as highly up-regulated genes in a mouse model of human lung adenocarcinoma. Overexpression of cathepsin proteases in these lung tumors was confirmed by immunohistochemistry and Western blotting. Therefore, an optical probe activated by cathepsin proteases was selected to detect murine lung tumors in vivo as small as 1 mm in diameter and spatially separated. We generated 3D maps of the fluorescence signal and fused them with anatomical computed tomography images to show a close correlation between fluorescence signal and tumor burden. By serially imaging the same mouse, optical imaging was used to follow tumor progression. This study demonstrates the capability for molecular imaging of a primary lung tumor by using endogenous proteases expressed by a tumor. It also highlights the feasibility of using gene expression profiling to identify molecular targets for imaging lung cancer.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1242291/
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4524
      1. Author :
        Takeshita, Fumitaka; Minakuchi, Yoshiko; Nagahara, Shunji; Honma, Kimi; Sasaki, Hideo; Hirai, Kotaro; Teratani, Takumi; Namatame, Nachi; Yamamoto, Yusuke; Hanai, Koji; Kato, Takashi; Sano, Akihiko; Ochiya, Takahiro
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2005
      5. Publication :
        Proceedings of the National Academy of Sciences of the United States of America
      6. Products :
      7. Volume :
        102
      8. Issue :
        34
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Animals; Bioware; Bone Neoplasms; Cell Line, Tumor; Collagen; DNA-Binding Proteins; Drug Carriers; Gene Expression Regulation, Neoplastic; Gene Therapy; Humans; Luciferases; Male; Mice; PC-3M-luc; Phosphatidylinositol 3-Kinases; Prostatic Neoplasms; Reverse Transcriptase Polymerase Chain Reaction; RNA, Small Interfering; Transcription Factors
      12. Abstract :
        Silencing of gene expression by small interfering RNAs (siRNAs) is rapidly becoming a powerful tool for genetic analysis and represents a potential strategy for therapeutic product development. However, there are no reports of systemic delivery for siRNAs toward treatment of bone-metastatic cancer. Accordingly, we report here that i.v. injection of GL3 luciferase siRNA complexed with atelocollagen showed effective reduction of luciferase expression from bone-metastatic prostate tumor cells developed in mouse thorax, jaws, and/or legs. We also show that the siRNA/atelocollagen complex can be efficiently delivered to tumors 24 h after injection and can exist intact at least for 3 days. Furthermore, atelocollagen-mediated systemic administration of siRNAs such as enhancer of zeste homolog 2 and phosphoinositide 3'-hydroxykinase p110-alpha-subunit, which were selected as candidate targets for inhibition of bone metastasis, resulted in an efficient inhibition of metastatic tumor growth in bone tissues. In addition, upregulation of serum IL-12 and IFN-alpha levels was not associated with the in vivo administration of the siRNA/atelocollagen complex. Thus, for treatment of bone metastasis of prostate cancer, an atelocollagen-mediated systemic delivery method could be a reliable and safe approach to the achievement of maximal function of siRNA.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/16091473
      14. Call Number :
        PKI @ catherine.lautenschlager @
      15. Serial :
        8979
      1. Author :
        Aki Hanyu; Kiyotsugu Kojima; Kiyohiko Hatake; Kimie Nomura; Hironori Murayama; Yuichi Ishikawa; Satoshi Miyata; Masaru Ushijima; Masaaki Matsuura; Etsuro Ogata; Keiji Miyazawa;Takeshi Imamura
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2009
      5. Publication :
        Cancer Science
      6. Products :
      7. Volume :
        100
      8. Issue :
        11
      9. Page Numbers :
        N/A
      10. Research Area :
        Cancer
      11. Keywords :
        Angiogenesis; metastasis; in vivo imaging; fluorescence imaging
      12. Abstract :
        Angiogenesis plays a crucial role in cancer progression and metastasis. Thus, blocking tumor angiogenesis is potentially a universal approach to prevent tumor establishment and metastasis. In this study, we used in vivo and ex vivo fluorescence imaging to show that an antihuman vascular endothelial growth factor (VEGF) antibody represses angiogenesis and the growth of primary tumors of human fibrosarcoma HT1080 cells in implanted nude mice. Interestingly, administering the antihuman VEGF antibody reduced the development of new blood vessels and normalized pre-existing tumor vasculature in HT1080 cell tumors. In addition, antihuman VEGF antibody treatment decreased lung metastasis from the primary tumor, whereas it failed to block lung metastasis in a lung colonization experiment in which tumor cells were injected into the tail vein. These results suggest that VEGF produced by primary HT1080 cell tumors has a crucial effect on lung metastasis. The present study indicates that the in vivo fluorescent microscopy system will be useful to investigate the biology of angiogenesis and test the effectiveness of angiogenesis inhibitors.
      13. URL :
        http://onlinelibrary.wiley.com/doi/10.1111/j.1349-7006.2009.01305.x/full
      14. Call Number :
        PKI @ sarah.piper @
      15. Serial :
        4495
      1. Author :
        BitMansour, A.; Burns, S. M.; Traver, D.; Akashi, K.; Contag, C. H.; Weissman, I. L.; Brown, J. M.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2002
      5. Publication :
        Blood
      6. Products :
      7. Volume :
        100
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Administration, Inhalation, Animals, Animals, Congenic, Aspergillosis/microbiology/*prevention & control, *Aspergillus fumigatus, Cell Lineage, Filgrastim/pharmacology, *Hematopoietic Stem Cell Transplantation, Injections, Intraperitoneal, Luminescent Measurements, Lung Diseases, Fungal/microbiology/*prevention & control, Mice, Mice, Inbred C57BL, Myeloid Progenitor Cells/physiology/*transplantation, Neutropenia/complications/drug therapy, Pseudomonas Infections/microbiology/*prevention & control, Radiation Chimera, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., Tissue Distribution IVIS, Xenogen, Xen5
      12. Abstract :
        Myelotoxic treatments for oncologic diseases are often complicated by neutropenia, which renders patients susceptible to potentially lethal infections. In these studies of murine hematopoietic stem cell transplantation (HSCT), cotransplantation of lineage-restricted progenitors known as common myeloid progenitors (CMP) and granulocyte-monocyte progenitors (GMP) protects against death following otherwise lethal challenge with either of 2 pathogens associated with neutropenia: Aspergillus fumigatus and Pseudomonas aeruginosa. Cotransplantation of CMP/GMP resulted in a significant and rapid increase in the absolute number of myeloid cells in the spleen, most of which were derived from the donor CMP/GMP. Despite persistent peripheral neutropenia, improved survival correlated with the measurable appearance of progenitor-derived myeloid cells in the spleen. A marked reduction or elimination of tissue pathogen load was confirmed by culture and correlated with survival. Localization of infection by P aeruginosa and extent of disease was also assessed by in vivo bioluminescent imaging using a strain of P aeruginosa engineered to constitutively express a bacterial luciferase. Imaging confirmed that transplantation with a graft containing hematopoietic stem cells and CMP/GMP reduced the bacterial load as early as 18 hours after infection. These results demonstrate that enhanced reconstitution of a tissue myeloid pool offers protection against lethal challenge with serious fungal and bacterial pathogens.
      13. URL :
        http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=12393415
      14. Call Number :
        136279
      15. Serial :
        7031
      1. Author :
        Malley, R.; Henneke, P.; Morse, S. C.; Cieslewicz, M. J.; Lipsitch, M.; Thompson, C. M.; Kurt-Jones, E.; Paton, J. C.; Wessels, M. R.; Golenbock, D. T.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2003
      5. Publication :
        Proceedings of the National Academy of Sciences of the United States of America
      6. Products :
      7. Volume :
        100
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS, Xenogen, Xen10
      12. Abstract :
        Streptococcus pneumoniae is one of the leading causes of invasive bacterial disease worldwide. Fragments of the cell wall and the cytolytic toxin pneumolysin have been shown to contribute substantially to inflammatory damage, although the interactions between pneumococcal components and host-cell structures have not been elucidated completely. Results of a previous study indicated that cell-wall components of pneumococci are recognized by Toll-like receptor (TLR)2 but suggested that pneumolysin induces inflammatory events independently of this receptor. In this study we tested the hypothesis that pneumolysin interacts with surface proteins of the TLR family other than TLR2. We found that pneumolysin stimulates tumor necrosis factor-? and IL-6 release in wild-type macrophages but not in macrophages from mice with a targeted deletion of the cytoplasmic TLR-adapter molecule myeloid differentiation factor 88, suggesting the involvement of the TLRs in pneumolysin recognition. Purified pneumolysin synergistically activated macrophage responses together with preparations of pneumococcal cell walls or staphylococcal peptidoglycan, which are known to activate TLR2. Furthermore, when compared with wild-type macrophages, macrophages from mice that carry a spontaneous mutation in TLR4 (P712H) were hyporesponsive to both pneumolysin alone and the combination of pneumolysin with pneumococcal cell walls. Finally, these TLR4-mutant mice were significantly more susceptible to lethal infection after intranasal colonization with pneumolysin-positive pneumococci than were control mice. We conclude that the interaction of pneumolysin with TLR4 is critically involved in the innate immune response to pneumococcus.
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/12569171
      14. Call Number :
        140854
      15. Serial :
        7487
      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 :
        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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