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Journal articles on the topic 'Murine model'

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Published: 4 June 2021
Last updated: 6 July 2024

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1

Libby, Peter. "Murine “Model” Monotheism." Circulation Research 117, no. 11 (November 6, 2015): 921–25. http://dx.doi.org/10.1161/circresaha.115.307523.

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2

Rodenberger, Sharon L., Philip W. Ledger, and Mary E. Prevo. "Murine Model for Contact Sensitization." Toxicology Methods 3, no. 3 (January 1993): 157–68. http://dx.doi.org/10.3109/15376519309044573.

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3

&NA;. "Alzheimer??s: murine model made." Inpharma Weekly &NA;, no. 975 (February 1995): 7. http://dx.doi.org/10.2165/00128413-199509750-00015.

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4

González, G. M., R. Tijerina, L. Najvar, M. Rinaldi, I. T. Yeh, and J. R. Graybill. "Experimental murine model of disseminatedPseudallescheriainfection." Medical Mycology 40, no. 3 (January 2002): 243–48. http://dx.doi.org/10.1080/mmy.40.3.243.248.

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5

Hofflin, J. M., F. K. Conley, and J. S. Remington. "Murine Model of Intracerebral Toxoplasmosis." Journal of Infectious Diseases 155, no. 3 (March 1, 1987): 550–57. http://dx.doi.org/10.1093/infdis/155.3.550.

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6

Chang, Christopher H., Peggy A. Cotter, and Jeff F. Miller. "Murine model of Campylobacter infection." Gastroenterology 118, no. 4 (April 2000): A322—A323. http://dx.doi.org/10.1016/s0016-5085(00)83382-x.

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7

Gronski, T., E. Lum, J. Campbell, and S. D. Shapiro. "A Murine Model of Volutrauma." Chest 116 (July 1999): 28S. http://dx.doi.org/10.1378/chest.116.suppl_1.28s.

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8

Ahmed, Abdalla O., Wim Vianen, Marian T. Kate, Wendy W. J. Sande, Alex Belkum, Ahmed H. Fahal, Henri A. Verbrugh, and Irma A. J. M. Bakker-Woudenberg. "A murine model ofMadurella mycetomatiseumycetoma." FEMS Immunology & Medical Microbiology 37, no. 1 (June 2003): 29–36. http://dx.doi.org/10.1016/s0928-8244(03)00096-8.

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9

LINDSAY, R., and W. BOLGER. "Murine Model of Chronic Rhinosinusitis." Otolaryngology - Head and Neck Surgery 133, no. 2 (August 2005): P103—P104. http://dx.doi.org/10.1016/j.otohns.2005.05.220.

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10

Gupta, Umesh Datta, Ali Abbas, Raj Pal Singh Kashyap, and Pushpa Gupta. "Murine model of TB meningitis." International Journal of Mycobacteriology 5 (December 2016): S178. http://dx.doi.org/10.1016/j.ijmyco.2016.10.029.

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11

Paredes, Katihuska, Javier Capilla, Deanna A. Sutton, Emilio Mayayo, Annette W. Fothergill, and Josep Guarro. "Virulence ofCurvulariain a murine model." Mycoses 56, no. 5 (February 26, 2013): 512–15. http://dx.doi.org/10.1111/myc.12064.

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12

ROBBINS, J. "The murine model of cardiogenesis." Journal of Molecular and Cellular Cardiology 23 (April 1991): S9. http://dx.doi.org/10.1016/0022-2828(91)91350-z.

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13

Feng, Fang, Nie Xingcao, and Li Ge. "A model system of primary murine hepatocytes infected by murine cytomegalovirus." Journal of Tongji Medical University 19, no. 3 (September 1999): 185–89. http://dx.doi.org/10.1007/bf02887730.

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14

Nogami, Makoto, Matsunobu Suko, Hirokazu Okudaira, Terumasa Miyamoto, Junji Shiga, and Shiro Kasuya. "A murine model of pulmonary eosinophilia." Ensho 9, no. 3 (1989): 205–8. http://dx.doi.org/10.2492/jsir1981.9.205.

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15

Savarese, John J., Bernd W. Brinken, and David J. Zaleske. "Epiphyseal Replacement in a Murine Model." Journal of Pediatric Orthopaedics 15, no. 5 (September 1995): 682–90. http://dx.doi.org/10.1097/01241398-199509000-00026.

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16

Hu, Calvin T., Sarah C. Offley, Zaneb Yaseen, Regis J. OʼKeefe, and Catherine A. Humphrey. "Murine Model of Oligotrophic Tibial Nonunion." Journal of Orthopaedic Trauma 25, no. 8 (August 2011): 500–505. http://dx.doi.org/10.1097/bot.0b013e3182249fad.

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17

Kumar, Rakesh K., and Paul S. Foster. "Murine model of chronic human asthma." Immunology & Cell Biology 79, no. 2 (April 2001): 141–44. http://dx.doi.org/10.1046/j.1440-1711.2001.00981.x.

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18

Smith, M. R., I. Joshi, F. Jin, and T. Al-Saleem. "Murine model for mantle cell lymphoma." Leukemia 20, no. 5 (March 9, 2006): 891–93. http://dx.doi.org/10.1038/sj.leu.2404177.

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19

Cooley, Brian C., and Roger A. Daley. "Murine Microvascular Anastomosis Model of Thrombosis." Thrombosis Research 96, no. 2 (October 1999): 157–59. http://dx.doi.org/10.1016/s0049-3848(99)00093-6.

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20

Ghosh, A., K. P. Leahy, S. Singhal, E. Einhorn, P. Howlett, N. A. Cohen, and N. Mirza. "A murine model of subglottic granulation." Journal of Laryngology & Otology 130, no. 4 (February 15, 2016): 380–87. http://dx.doi.org/10.1017/s0022215116000049.

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AbstractObjective:This study aimed to develop a functional model of subglottic stenosis by inducing direct airway irritation in transplanted mouse laryngotracheal complexes.Methods:Laryngotracheal complexes from C57BL/6 mice were harvested and divided into three groups: uninjured, mechanically injured and chemically injured. Donor laryngotracheal complexes from each group were placed in dorsal subcutaneous pockets of recipient mice. Each week, the transplanted laryngotracheal complexes were harvested, and tissues were fixed, sectioned, and stained with haematoxylin and eosin. Representative slides were reviewed by a blinded pathologist, to determine the formation of granulation tissue, and graded as to the degree of granulation formation.Results:Direct airway irritation induced granulation tissue formation under the disrupted epithelium of airway mucosa; this was seen as early as two weeks after chemical injury.Conclusion:Results indicate that granulation tissue formation in a murine model may be an efficient tool for investigating the development and treatment of subglottic stenosis.
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21

Bates, J. N., R. L. Davisson, D. S. Hoffmann, G. M. Butz, G. Aldape, G. Schlager, D. C. Merrill, S. Sethi, and R. M. Weiss. "A MURINE MODEL OF SPONTANEOUS PREECLAMPSIA." Anesthesiology 96, no. 4 (April 1, 2002): NA. http://dx.doi.org/10.1097/00000542-200204001-00019.

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22

Graber, T., B. Rawls, B. Tian, W. Durham, A. Brasier, B. Rasmussen, and C. Fry. "COPD CACHEXIA IN A MURINE MODEL." Innovation in Aging 1, suppl_1 (June 30, 2017): 425–26. http://dx.doi.org/10.1093/geroni/igx004.1529.

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23

Abram, Maja, Dirk Schlüter, Darinka Vuckovic, Branka Wraber, Miljenko Doric, and Martina Deckert. "Murine model of pregnancy-associatedListeria monocytogenesinfection." FEMS Immunology & Medical Microbiology 35, no. 3 (April 2003): 177–82. http://dx.doi.org/10.1016/s0928-8244(02)00449-2.

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24

Isefuku, S., C. J. Joyner, and A. H. R. W. Simpson. "A murine model of distraction osteogenesis." Bone 27, no. 5 (November 2000): 661–65. http://dx.doi.org/10.1016/s8756-3282(00)00385-9.

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25

Parti, Rajinder P. S., Sudhir Srivastava, Ratan Gachhui, Kishore K. Srivastava, and Ranjana Srivastava. "Murine infection model for Mycobacterium fortuitum." Microbes and Infection 7, no. 3 (March 2005): 349–55. http://dx.doi.org/10.1016/j.micinf.2004.11.006.

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26

Jones, W. Keith. "A Murine Model of Alcoholic Cardiomyopathy." American Journal of Pathology 167, no. 2 (August 2005): 301–4. http://dx.doi.org/10.1016/s0002-9440(10)62975-6.

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27

Peck, M. A., H. Albadawi, R. S. Crawford, H. Yoo, C. J. Abularrage, V. I. Patel, M. F. Conrad, and M. T. Watkins. "QS413. A Murine Model of Claudication." Journal of Surgical Research 151, no. 2 (February 2009): 301. http://dx.doi.org/10.1016/j.jss.2008.11.725.

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28

Rikhi, Rishi, Elizabeth M. Wilson, Olivier Deas, Matthew N. Svalina, John Bial, Atiya Mansoor, Stefano Cairo, and Charles Keller. "Murine model of hepatic breast cancer." Biochemistry and Biophysics Reports 8 (December 2016): 1–5. http://dx.doi.org/10.1016/j.bbrep.2016.07.021.

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29

Padilla-Fernández, B., M. B. García-Cenador, P. Rodríguez-Marcos, J. F. López-Marcos, P. Antúnez-Plaza, J. M. Silva-Abuín, D. López-Montañés, F. J. García-Criado, and M. F. Lorenzo-Gómez. "Experimental murine model of renal cancer." Actas Urológicas Españolas (English Edition) 41, no. 7 (September 2017): 445–50. http://dx.doi.org/10.1016/j.acuroe.2017.06.003.

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30

Chao, Chun C., Michael DeLaHunt, Shuxian Hu, Karen Close, and Phillip K. Peterson. "Immunologically mediated fatigue: A murine model." Clinical Immunology and Immunopathology 64, no. 2 (August 1992): 161–65. http://dx.doi.org/10.1016/0090-1229(92)90194-s.

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31

Horton, J., J. White, D. Maass, B. Sanders, J. Murphy, and B. Giroir. "A MURINE MODEL OF BURN TRAUMA." Shock 11, Supplement (June 1999): 2. http://dx.doi.org/10.1097/00024382-199906001-00008.

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32

Matthew, E., G. Warden, and J. Dedman. "A murine model of smoke inhalation." American Journal of Physiology-Lung Cellular and Molecular Physiology 280, no. 4 (April 1, 2001): L716—L723. http://dx.doi.org/10.1152/ajplung.2001.280.4.l716.

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The United States has one of the world's largest per capita fire death rates. House fires alone kill >9,000 Americans annually, and smoke inhalation is the leading cause of mortality from structural fires. Animal models are needed to develop therapies to combat this problem. We have developed a murine model of smoke inhalation through the design, construction, and use of a controlled-environment smoke chamber. There is a direct relationship between the quantity of wood combusted and mortality in mice. As with human victims, the primary cause of death from smoke inhalation is an elevated blood carboxyhemoglobin level. Lethal (78%) and sublethal (50%) carboxyhemoglobin levels were obtained in mice subjected to varying amounts of smoke. Mice exposed to wood smoke demonstrated more dramatic pathology than mice exposed to cotton or polyurethane smoke. A CD-1 model of wood smoke exposure was developed, demonstrating type II cell hypertrophy, cytoplasmic blebbing, cytoplasmic vacuolization, sloughing, hemorrhage, edema, macrophage infiltration, and lymphocyte infiltration. The bronchoalveolar lavage fluid of smoke-exposed mice demonstrated a significant increase in total cell counts compared with those in control mice. These findings are comparable to the lung tissue response observed in human victims of smoke inhalation.
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33

Snouwaert, John N., Kristen K. Brigman, Anne M. Latour, Elizabeth Iraj, Ute Schwab, Matthew Ian Gilmour, and Beverly H. Koller. "A Murine Model of Cystic Fibrosis." American Journal of Respiratory and Critical Care Medicine 151, no. 3_pt_2 (March 1995): S59—S64. http://dx.doi.org/10.1164/ajrccm/151.3_pt_2.s59.

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34

Altuntas, C. Z., L. N. Byrne, B. Bakhautdin, C. Sakalar, P. L. Fox, V. K. Tuohy, and F. Daneshgari. "648 NOVEL MURINE EXPERIMENTAL PROSTATITIS MODEL." European Urology Supplements 9, no. 2 (April 2010): 215. http://dx.doi.org/10.1016/s1569-9056(10)60637-9.

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35

Chan, C. C., M. Fischette, D. Shen, S. P. Mahesh, R. B. Nussenblat, and J. Hochman. "Murine model of primary intraocular lymphoma." American Journal of Ophthalmology 139, no. 5 (May 2005): 957. http://dx.doi.org/10.1016/j.ajo.2005.03.010.

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36

Kamberi, Perparim, Raymond A. Sobel, Karl V. Clemons, David A. Stevens, Demosthenes Pappagianis, and Paul L. Williams. "A Murine Model of Coccidioidal Meningitis." Journal of Infectious Diseases 187, no. 3 (February 2003): 453–60. http://dx.doi.org/10.1086/367961.

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37

Crnej, Alja, Masahiro Omoto, Thomas H. Dohlman, John M. Graney, Claes H. Dohlman, Brigita Drnovsek-Olup, and Reza Dana. "A Novel Murine Model for Keratoprosthesis." Investigative Opthalmology & Visual Science 55, no. 6 (June 13, 2014): 3681. http://dx.doi.org/10.1167/iovs.14-14058.

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38

Chan, Chi-Chao, Maria Fischette, DeFen Shen, Sankaranarayana P. Mahesh, Robert B. Nussenblatt, and Jacob Hochman. "Murine Model of Primary Intraocular Lymphoma." Investigative Opthalmology & Visual Science 46, no. 2 (February 1, 2005): 415. http://dx.doi.org/10.1167/iovs.04-0869.

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39

Shi, C., M. E. Russell, C. Bianchi, J. B. Newell, and E. Haber. "Murine model of accelerated transplant arteriosclerosis." Circulation Research 75, no. 2 (August 1994): 199–207. http://dx.doi.org/10.1161/01.res.75.2.199.

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40

Fernandez, Christian A., Colton Smith, Seth E. Karol, Laura B. Ramsey, Chengcheng Liu, Ching-Hon Pui, Sima Jeha, William E. Evans, Fred D. Finkelman, and Mary V. Relling. "A Murine Model of Asparaginase Allergy." Blood 124, no. 21 (December 6, 2014): 2295. http://dx.doi.org/10.1182/blood.v124.21.2295.2295.

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Abstract In order to study interventions that influence the severity of symptoms and serum asparaginase activity following asparaginase-induced hypersensitivity reactions, we developed a murine model of asparaginase allergy that recapitulates key features of clinical hypersensitivity to native E. coli asparaginase. BALB/c mice received 10 μg ip doses of E. coli asparaginase formulated with aluminum hydroxide adjuvant on day 0 and 14 of treatment in order to sensitize mice to asparaginase. Asparaginase allergies were induced in sensitized mice by challenging with a 100 μg iv dose of E. coli asparaginase on day 24 of treatment. The severity of hypersensitivity was reflected by the decrease in rectal temperature following the asparaginase challenge. Pre-challenge plasma samples were collected for anti-asparaginase antibody levels before inducing asparaginase allergies, and post-challenge samples were collected at the end of the experiment for measuring anti-asparaginase antibody levels, asparaginase activity, and mouse mast cell protease 1 (mMCP-1) levels. Sensitized mice developed high levels of anti-asparaginase IgG antibodies (P = 1.1 x 10-7) and had immediate hypersensitivity reactions (P = 3.3 x 10-10) to asparaginase upon challenge compared to non-sensitized mice. Furthermore, sensitized mice had profoundly lower plasma asparaginase activity (P = 4.2 x 10-13) and elevated levels of mouse mast cell protease 1 (mMCP-1, P = 6.1 x 10-3) after the asparaginase challenge compared to non-sensitized mice. We investigated the influence of pretreatment with the H1 receptor antagonist triprolidine, the H2 receptor antagonist cimetidine, the PAF receptor antagonist CV-6209, or dexamethasone on the severity of asparaginase-induced allergies. Our studies showed that the combination of triprolidine and CV-6209 was best for mitigating asparaginase-induced hypersensitivity symptoms (i.e., temperature drop) compared to non-pretreated, sensitized mice (P = 1.2 x 10-5). However, pretreatment with oral dexamethasone (4 mg/L in drinking water starting 7 days before asparaginase sensitization) was the only agent capable of mitigating the severity of the hypersensitivity symptoms (P = 0.03) and also partially restoring asparaginase activity (P = 8.3 x 10-4) compared to sensitized mice. Dose adjustment strategies were investigated for rescuing asparaginase activity in sensitized mice without requiring pretreatment with dexamethasone, and a 5-fold greater dose of asparaginase was required to restore enzyme activity to a similar concentration as in non-sensitized mice. In the absence of pretreatment, we found that the severity of asparaginase-induced reactions increased in a dose-dependent manner and that mMCP-1 levels correlated to the severity of the reactions (R2 = 0.577, P = 3.0 x 10-16). Our results suggest a role of histamine and PAF in asparaginase-induced allergies and demonstrate possible strategies for mitigating the severity of asparaginase-induced reactions and maintaining targeted concentrations of asparaginase. Furthermore, our results indicate that mast cell-derived proteases released during allergic reactions to asparaginase may be a useful marker of hypersensitivity, as elevated levels of mMCP-1 were detected in all sensitized mice and correlated with the severity of the reaction. Disclosures Evans: St. Jude: In accordance with institutional policy (St. Jude), I and/or my spouse have in the past received a portion of the income St. Jude receives from licensing patent rights related to TPMT polymorphisms as clinical diagnostics. Patents & Royalties. Relling:St. Jude: In accordance with institutional policy (St. Jude), I and/or my spouse have in the past received a portion of the income St. Jude receives from licensing patent rights related to TPMT polymorphisms as clinical diagnostics. Patents & Royalties.
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41

Johnson, Bryon D. "Exciting new murine model of cGVHD." Blood 119, no. 6 (February 9, 2012): 1331–32. http://dx.doi.org/10.1182/blood-2011-12-393496.

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42

Jerrells, Thomas R., Wiley Smith, and Michael J. Eckardt. "Murine Model of Ethanol-Induced Immunosuppression." Alcoholism: Clinical and Experimental Research 14, no. 4 (August 1990): 546–50. http://dx.doi.org/10.1111/j.1530-0277.1990.tb01197.x.

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43

Loving, Crystal L., Mary Kennett, Gloria M. Lee, Vanessa K. Grippe, and Tod J. Merkel. "Murine Aerosol Challenge Model of Anthrax." Infection and Immunity 75, no. 6 (March 12, 2007): 2689–98. http://dx.doi.org/10.1128/iai.01875-06.

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ABSTRACT The availability of relevant and useful animal models is critical for progress in the development of effective vaccines and therapeutics. The infection of rabbits and non-human primates with fully virulent Bacillus anthracis spores provides two excellent models of anthrax disease. However, the high cost of procuring and housing these animals and the specialized facilities required to deliver fully virulent spores limit their practical use in early stages of product development. Conversely, the small size and low cost associated with using mice makes this animal model more practical for conducting experiments in which large numbers of animals are required. In addition, the availability of knockout strains and well-characterized immunological reagents makes it possible to perform studies in mice that cannot be performed easily in other species. Although we, along with others, have used the mouse aerosol challenge model to examine the outcome of B. anthracis infection, a detailed characterization of the disease is lacking. The current study utilizes a murine aerosol challenge model to investigate disease progression, innate cytokine responses, and histological changes during the course of anthrax after challenge with aerosolized spores. Our results show that anthrax disease progression in a complement-deficient mouse after challenge with aerosolized Sterne spores is similar to that described for other species, including rabbits and non-human primates, challenged with fully virulent B. anthracis. Thus, the murine aerosol challenge model is both useful and relevant and provides a means to further investigate the host response and mechanisms of B. anthracis pathogenesis.
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44

Mayuzumi, H., Y. Ohki, K. Tokuyama, T. Mizuno, H. Arakawa, H. Mochizuki, and A. Morikawa. "A Murine Model Of Childhood Asthma." Journal of Allergy and Clinical Immunology 119, no. 1 (January 2007): S129. http://dx.doi.org/10.1016/j.jaci.2006.11.488.

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45

Elkhal, A., J. Scott, D. H. MacArthur, R. He, M. D. Howell, E. Freyschmidt, H. C. Oettgen, D. Y. M. Leung, and R. S. Geha. "A Murine Model of Eczema Vaccinatum." Journal of Allergy and Clinical Immunology 119, no. 1 (January 2007): S201. http://dx.doi.org/10.1016/j.jaci.2006.12.157.

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46

Cooley, Brian C. "Model of murine interpositional vein grafting." Microsurgery 25, no. 3 (2005): 209–12. http://dx.doi.org/10.1002/micr.20106.

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47

Eller, Philipp, Kathrin Eller, Alexander H. Kirsch, Josef J. Patsch, Anna M. Wolf, Andrea Tagwerker, Ursula Stanzl, et al. "A Murine Model of Phosphate Nephropathy." American Journal of Pathology 178, no. 5 (May 2011): 1999–2006. http://dx.doi.org/10.1016/j.ajpath.2011.01.024.

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48

Day, Sharlene, Jennifer Reeve, Daniel Myers, and William Fay. "Murine thrombosis models." Thrombosis and Haemostasis 92, no. 09 (2004): 486–94. http://dx.doi.org/10.1055/s-0037-1613739.

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SummaryDue to exciting advances in molecular biology, the laboratory mouse has become an important and frequently used model for studying thrombosis. This article reviews several experimental approaches that have been used to study arterial, venous, and microvascular thrombosis in mice. The advantages and limitations of different models are examined. Related topics of mouse anesthesia, phlebotomy, and in vitro hemostasis testing are also reviewed.
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49

Christadoss, P., and M. J. Dauphinee. "Immunotherapy for myasthenia gravis: a murine model." Journal of Immunology 136, no. 7 (April 1, 1986): 2437–40. http://dx.doi.org/10.4049/jimmunol.136.7.2437.

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Abstract In vivo therapy with monoclonal antibody (mAb) GK1.5, which recognizes a glycoprotein antigen designated L3T4 on murine helper T lymphocytes, either prevented or suppressed the development of murine lupus, autoimmune encephalomyelitis, and collagen arthritis. The L3T4 antigen in the mouse is analogous to the human Leu-3/T4 antigen expressed on helper T lymphocytes, because they both participate in the T cell response to class II major histocompatibility complex (MHC) antigens. Class II MHC genes and I-A antigens mediate murine experimental autoimmune myasthenia gravis (EAMG) induced by acetylcholine receptor (AChR) autoimmunity. We studied the efficacy of mAb GK1.5 as an immunotherapeutic agent for murine EAMG. Therapy with mAb GK1.5 not only suppressed established autoimmunity to AChR but also prevented loss of muscle AChR in mice with EAMG. Moreover, permanent remission of clinical muscle weakness was induced if mAb GK1.5 therapy was initiated after the onset of clinical disease. Because the function of the Leu-3/T4 determinant on human helper T lymphocytes is analogous to the murine L3T4 determinant, use of antibody to the Leu-3/T4 determinant as an immunotherapeutic agent may provide a way to control the progression of human MG.
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50

Benson, Robert A., Iain B. McInnes, Paul Garside, and James M. Brewer. "Model answers: Rational application of murine models in arthritis research." European Journal of Immunology 48, no. 1 (December 14, 2017): 32–38. http://dx.doi.org/10.1002/eji.201746938.

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