The Experts below are selected from a list of 550179 Experts worldwide ranked by ideXlab platform
Roberto Cevenini - One of the best experts on this subject based on the ideXlab platform.
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A Mouse Model for Chlamydia suis genital infection.
Pathogens and disease, 2014Co-Authors: Manuela Donati, Antonietta Di Francesco, Maria Di Paolo, Alison Favaroni, Rita Aldini, Fabio Ostanello, Roberta Biondi, Eleonora Cremonini, Laura Ginocchietti, Roberto CeveniniAbstract:A Mouse Model for Chlamydia suis genital infection was developed. Ninety-nine mice were randomly divided into three groups and intravaginally inoculated with chlamydia: 45 mice (group 1) received C. suis purified elementary bodies (EBs), 27 (group 2) were inoculated with C. trachomatis genotype E EBs and 27 mice (group 3) with C. trachomatis genotype F EBs. Additionally, 10 mice were used as a negative control. At seven days post-infection (dpi) secretory anti- C. suis IgA were recovered from vaginal swabs of all C. suis inoculated mice. Chlamydia suis was isolated from 93, 84, 71 and 33% vaginal swabs at 3, 5, 7 and 12 dpi. Chlamydia trachomatis genotype E and F were isolated from 100% vaginal swabs up to 7 dpi and from 61 and 72%, respectively, at 12 dpi. Viable C. suis and C. trachomatis organisms were isolated from uterus and tubes up to 16 and 28 dpi, respectively. The results of the present study show the susceptibility of mice to intravaginal inoculation with C. suis . A more rapid course and resolution of C. suis infection, in comparison to C. trachomatis , was highlighted. The Mouse Model could be useful for comparative investigations involving C. suis and C. trachomatis species.
Claire Greenhill - One of the best experts on this subject based on the ideXlab platform.
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Ulcerative colitis: Mouse Model reveals how appendicitis protects against ulcerative colitis.
Nature reviews. Gastroenterology & hepatology, 2014Co-Authors: Claire GreenhillAbstract:Ulcerative colitis: Mouse Model reveals how appendicitis protects against ulcerative colitis
Joel E. Michalek - One of the best experts on this subject based on the ideXlab platform.
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Preclinical Testing of Erlotinib in a Transgenic Alveolar Rhabdomyosarcoma Mouse Model
Sarcoma, 2011Co-Authors: Jinu Abraham, Laura D. Nelon, Courtney B. Kubicek, Sheila T. Hampton, Lee Ann Zarzabal, Joel E. Michalek, Brian P Rubin, Aoife Kilcoyne, Francis J Giles, Charles KellerAbstract:Rhabdomyosarcoma is an aggressive childhood malignancy, accounting for more than 50% of all soft-tissue sarcomas in children. Even with extensive therapy, the survival rate among alveolar rhabdomyosarcoma patients with advanced disease is only 20%. The receptor tyrosine kinase Epidermal Growth Factor Receptor (EGFR) has been found to be expressed and activated in human rhabdomyosarcomas. In this study we have used a genetically engineered Mouse Model for alveolar rhabdomyosarcoma (ARMS) which faithfully recapitulates the human disease by activating the pathognomic Pax3:Fkhr fusion gene and inactivating p53 in the maturing myoblasts. We have demonstrated that tumors from our Mouse Model of alveolar rhabdomyosarcoma express EGFR at both the mRNA and protein levels. We then tested the EGFR inhibitor, Erlotinib, for its efficacy in this Mouse Model of alveolar rhabdomyosarcoma. Surprisingly, Erlotinib had no effect on tumor progression, yet mice treated with Erlotinib showed 10–20% loss of body weight. These results suggest that EGFR might not be an a priori monotherapy target in alveolar rhabdomyosarcoma.
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credentialing a preclinical Mouse Model of alveolar rhabdomyosarcoma
Cancer Research, 2009Co-Authors: Koichi Nishijo, Lei Zhang, Qingrong Chen, Amanda T Mccleish, Andrea Rodriguez, Suresh I Prajapati, Jonathan A L Gelfond, Gary B Chisholm, Joel E. MichalekAbstract:The highly aggressive muscle cancer alveolar rhabdomyosarcoma (ARMS) is one of the most common soft tissue sarcoma of childhood, yet the outcome for the unresectable and metastatic disease is dismal and unchanged for nearly three decades. To better understand the pathogenesis of this disease and to facilitate novel preclinical approaches, we previously developed a conditional Mouse Model of ARMS by faithfully recapitulating the genetic mutations observed in the human disease, i.e., activation of Pax3:Fkhr fusion gene with either p53 or Cdkn2a inactivation. In this report, we show that this Model recapitulates the immunohistochemical profile and the rapid progression of the human disease. We show that Pax3:Fkhr expression increases during late preneoplasia but tumor cells undergoing metastasis are under apparent selection for Pax3:Fkhr expression. At a whole-genome level, a cross-species gene set enrichment analysis and metagene projection study showed that our Mouse Model is most similar to human ARMS when compared with other pediatric cancers. We have defined an expression profile conserved between Mouse and human ARMS, as well as a Pax3:Fkhr signature, including the target gene, SKP2. We further identified 7 “druggable” kinases overexpressed across species. The data affirm the accuracy of this genetically engineered Mouse Model. [Cancer Res 2009;69(7):2902–11]
M. Eveillard - One of the best experts on this subject based on the ideXlab platform.
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Colistin–glycopeptide combinations against multidrug-resistant Acinetobacter baumannii in a Mouse Model of pneumonia
Future Microbiology, 2019Co-Authors: D. Sanderink, V. Cassisa, R. Chenouard, R. Mahieu, M. Kempf, V. Dubée, M. EveillardAbstract:Aim: To assess the effect of colistin-glycopeptide combination against a multidrug-resistant strain of Acinetobacter baumannii. Materials & methods: We used in vitro procedures (Etest method, checkerboard test and kill-time assays) and a Mouse Model of a carbapenem-resistant A. baumannii pneumonia. Results: The colistin-teicoplanin combination allowed a 74% increase of the survival in the Mouse Model within the 4 days following bacterial inoculation as compared with saline or colistin alone (p = 0.06). Concurrently, the colistin-vancomycin combination presented a similar efficacy as compared with saline or colistin alone in the Mouse Model. Conclusion: According to those preliminary results, using the colistin-teicoplanin combination in therapeutic deadlocks encountered in certain multiresistant A. baumannii pneumonia could be envisaged if the results are confirmed.
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Colistin-glycopeptide combinations against multidrug-resistant in a Mouse Model of pneumonia
'Future Medicine Ltd', 2019Co-Authors: D. Sanderink, V. Cassisa, R. Chenouard, R. Mahieu, M. Kempf, V. Dubée, M. EveillardAbstract:To assess the effect of colistin-glycopeptide combination against a multidrug-resistant strain of . We used procedures (Etest method, checkerboard test and kill-time assays) and a Mouse Model of a carbapenem-resistant pneumonia. The colistin-teicoplanin combination allowed a 74% increase of the survival in the Mouse Model within the 4 days following bacterial inoculation as compared with saline or colistin alone (p = 0.06). Concurrently, the colistin-vancomycin combination presented a similar efficacy as compared with saline or colistin alone in the Mouse Model. According to those preliminary results, using the colistin-teicoplanin combination in therapeutic deadlocks encountered in certain multiresistant pneumonia could be envisaged if the results are confirmed
Thomas W. Geisbert - One of the best experts on this subject based on the ideXlab platform.
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Lymphocyte Death in a Mouse Model of Ebola Virus Infection
The Journal of Infectious Diseases, 2007Co-Authors: Denise R. Braun, Jason Paragas, Aura R Garrison, Joan B. Geisbert, Lisa E. Hensley, Joshua D. Shamblin, Thomas W. GeisbertAbstract:Background. A striking feature of Zaire Ebola virus (ZEBOV) infection in nonhuman primates is the rapid depletion of T and NK lymphocytes by apoptosis. In a Mouse Model of ZEBOV infection, lymphocyte death is a prominent finding; however, the mechanism of death and the lymphocyte subsets that are targeted remain unknown. Methods. We extended the characterization of lymphocyte death in a Mouse Model of ZEBOV infection by evaluating lymphocytes during the course of disease, using flow cytometry, electron microscopy, and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL). Results. B cell, CD4 + and CD8 + T cell, and NK cell counts all dropped dramatically in the blood of infected BALB/c mice, and lymphocyte death was observed in the spleen by means of TUNEL staining and in the blood by means of electron microscopy. Morphologically, lymphocyte death occurred by both classic apoptosis and apoptosis-like programmed cell death. Conclusions. The early and severe loss of peripheral blood NK and CD8 + lymphocytes in ZEBOV-infected mice is similar to that seen in macaques. The morphological basis of lymphocyte death in ZEBOV-infected mice appears to be both classic apoptosis and apoptosis-like programmed cell death, although lymphocyte apoptosis in ZEBOV-infected nonhuman primates seems to occur primarily via classic apoptosis. The Mouse Model of ZEBOV infection may be useful for the screening of therapeutics directed against limiting lymphocyte death.
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Lymphocyte death in a Mouse Model of Ebola virus infection.
The Journal of infectious diseases, 2007Co-Authors: Denise R. Braun, Jason Paragas, Joan B. Geisbert, Lisa E. Hensley, Joshua D. Shamblin, Aura Garrison, Thomas W. GeisbertAbstract:A striking feature of Zaire Ebola virus (ZEBOV) infection in nonhuman primates is the rapid depletion of T and NK lymphocytes by apoptosis. In a Mouse Model of ZEBOV infection, lymphocyte death is a prominent finding; however, the mechanism of death and the lymphocyte subsets that are targeted remain unknown. We extended the characterization of lymphocyte death in a Mouse Model of ZEBOV infection by evaluating lymphocytes during the course of disease, using flow cytometry, electron microscopy, and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL). B cell, CD4+ and CD8+ T cell, and NK cell counts all dropped dramatically in the blood of infected BALB/c mice, and lymphocyte death was observed in the spleen by means of TUNEL staining and in the blood by means of electron microscopy. Morphologically, lymphocyte death occurred by both classic apoptosis and apoptosis-like programmed cell death. The early and severe loss of peripheral blood NK and CD8+ lymphocytes in ZEBOV-infected mice is similar to that seen in macaques. The morphological basis of lymphocyte death in ZEBOV-infected mice appears to be both classic apoptosis and apoptosis-like programmed cell death, although lymphocyte apoptosis in ZEBOV-infected nonhuman primates seems to occur primarily via classic apoptosis. The Mouse Model of ZEBOV infection may be useful for the screening of therapeutics directed against limiting lymphocyte death.
