Relevant bibliographies by topics / Murine mode

Academic literature on the topic 'Murine mode'

Author: Grafiati
Published: 7 July 2024
Last updated: 7 July 2024

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Journal articles on the topic "Murine mode":

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Itoh, Masahiro, Hiroshi Moriyama, Akiko Yano, Xiu-Qin Li, and Yoshiki Takeuchi. "Mode of migration of normal lymphocytes inside murine testis." Anatomical Record 251, no. 2 (June 1998): 152–60. http://dx.doi.org/10.1002/(sici)1097-0185(199806)251:2<152::aid-ar2>3.0.co;2-0.

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Arakawa, Tsutomu, Yasunori Kurosawa, Michael Storms, Toshiaki Maruyama, C. J. Okumura, and Yoshiko Kita. "Capto MMC mixed-mode chromatography of murine and rabbit antibodies." Protein Expression and Purification 127 (November 2016): 105–10. http://dx.doi.org/10.1016/j.pep.2016.07.010.

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Fabre, Pierre-Henri, Yuli S. Fitriana, Gono Semiadi, Marie Pagès, Ken Aplin, Nanang Supriatna, and Kristofer M. Helgen. "New record of Melomys burtoni (Mammalia, Rodentia, Murinae) from Halmahera (North Moluccas, Indonesia): a review of Moluccan Melomys." Mammalia 82, no. 3 (April 25, 2018): 218–47. http://dx.doi.org/10.1515/mammalia-2016-0137.

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AbstractMosaic-tailed rodents of the genusMelomysbelong to the Australasian old endemic murine radiation and exhibit a rat-like morphology with arboreal or scansorial specializations. Here we report a new population ofMelomys burtonifrom the island of Halmahera (in the North Moluccas, Indonesia). Our molecular phylogenetic results highlight close relationships and recent evolutionary divergences amongM. burtonifrom Halmahera and the Australo-Papuan taxaM. burtoniandM. lutillusand other Moluccan taxa, includingM. paveli. Multivariate as well as geometric morphometric analyses of cranial, and dental features support the recognition ofM. burtonifrom Halmahera as a slightly distinctive insular population, preventing us from elevating it as a new taxa. This population is recorded from lowland secondary forest and forest edge habitats in south-central Halmahera. As with other Moluccan endemic murines, colonization by an Australo-Papuan ancestor and subsequent isolation is the probable mode of diversification forM. burtoniin Halmahera. The discovery ofMelomysin Halmahera fills a previously puzzling gap in knowledge of the murine fauna of the Moluccas and the biogeography of the Wallacean region.
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Kolpakov, Sergei, Elena Kolpakova, Elena Zlatnik, Evgeniya Nepomnyashchaya, Inna Novikova, Oksana Shulgina, Alexandr Sagakyants, and Yuri Sidorenko. "Evaluation of antitumor activity in strains of a new rotavirus group in Reoviridae family on a model of transplantable murine melanoma." Problems in oncology 66, no. 6 (December 30, 2020): 712–17. http://dx.doi.org/10.37469/0507-3758-2020-66-6-712-717.

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The purpose was to study antitumor effects of the group K rotaviruses strains No. 228 and No. 100 in the experiment on a model of transplantable murine melanoma. Material and methods. The study included 65 С57Black/6 mice with transplantable B16/F10 melanoma and two strains of the Reoviridae family members characterized as rotaviruses, not belonging to the known groups, with the working title “group K rotaviruses (RVK)”. Animals received RVK in “vaccination” (before tumor transplantation) and “treatment” (after tumor formation) modes. Live and inactivated strains were used. RVK were administered intramuscularly as 0.3 ml of virus-containing culture fluid with at least 5x109 viral particles per 1 ml, with a total of 4 injections. Life span of mice and morphological characteristics of tumors were evaluated. Results. Injections of both strains increased the survival of tumor-bearing mice by 1.7-1.9 times in 4 of 8 experimental groups, compared to controls. The modes of RVK administration showed some differences: the survival was longer in mice with the “vaccination” mode compared to the “treatment” mode. Morphological changes in tumors were similar after application of both modes and inclued dystrophic changes of tumor cells, formation of extensive necrosis areas, and leukocyte infiltration. Discussion. Live and inactivated RVK had unidirectional effects implying its association with immunomodulatory action rather than with a direct lytic effect on the tumor. Conclusions. Both studied strains of rotaviruses in the group K had antitumor effect in the model of transplantable В16/F10 murine melanoma in the «vaccination» mode.
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Prabhakara, Ranjani, Janette M. Harro, Jeff G. Leid, Megan Harris, and Mark E. Shirtliff. "Murine Immune Response to a ChronicStaphylococcus aureusBiofilm Infection." Infection and Immunity 79, no. 4 (January 31, 2011): 1789–96. http://dx.doi.org/10.1128/iai.01386-10.

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ABSTRACTStaphylococcus aureushas reemerged as an important human pathogen in recent decades. Although many infections caused by this microbial species persist through a biofilm mode of growth, little is known about how the host's adaptive immune system responds to these biofilm infections. In this study,S. aureuscells adhered to pins in culture and were subsequently inserted into the tibiae of C57BL/6 mice, with an infecting dose of 2 × 105CFU. This model was utilized to determine local cytokine levels, antibody (Ab) function, and T cell populations at multiple time points throughout infection. Like human hosts,S. aureusimplant infection was chronic and remained localized in 100% of C57BL/6 mice at a consistent level of approximately 107CFU/gram bone tissue after day 7. This infection persisted locally for >49 days and was recalcitrant to clearance by the host immune response and antimicrobial therapy. Local inflammatory cytokines of the Th1 (interleukin-2 [IL-2], IL-12 p70, tumor necrosis factor alpha [TNF-α], and IL-1β) and Th17 (IL-6 and IL-17) responses were upregulated throughout the infection, except IL-12 p70, which dwindled late in the infection. In addition, Th1 Ab subtypes against a biofilm antigen (SA0486) were upregulated early in the infection, while Th2 Abs and anti-inflammatory regulatory T cells (Tregs) were not upregulated until later. These results indicate that early Th1 and Th17 inflammatory responses and downregulated Th2 and Treg responses occur during the development of a chronic biofilm implant infection. This unrestrained inflammatory response may cause tissue damage, thereby enablingS. aureusto attach and thrive in a biofilm mode of growth.
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Gareau, Daniel S., Glenn Merlino, Christopher Corless, Molly Kulesz-Martin, and Steven L. Jacques. "Noninvasive Imaging of Melanoma with Reflectance Mode Confocal Scanning Laser Microscopy in a Murine Model." Journal of Investigative Dermatology 127, no. 9 (September 2007): 2184–90. http://dx.doi.org/10.1038/sj.jid.5700829.

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Poole, Aaron, Phyllis Gamble, Esther Tamayo, Igor Patrikeev, Jingna Wei, Kathleen Vinvent, Gayle Olson, George Saade, Alison Stuebe, and Egle Bytautiene. "41: Effect of lactation on maternal postpartum cardiometabolic status–a murine mode." American Journal of Obstetrics and Gynecology 210, no. 1 (January 2014): S27. http://dx.doi.org/10.1016/j.ajog.2013.10.074.

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Li, Pei-Lin, Rodger E. Tiedemann, S. Louise Moffat, and John D. Fraser. "The Superantigen Streptococcal Pyrogenic Exotoxin C (SPE-C) Exhibits a Novel Mode of Action." Journal of Experimental Medicine 186, no. 3 (August 4, 1997): 375–83. http://dx.doi.org/10.1084/jem.186.3.375.

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Recombinant streptococcal pyrogenic exotoxin C (SPE-C) is a potent superantigen that stimulates Vβ2-bearing human T cells, but is inactive in mice. SPE-C binds with high affinity to both human HLA-DR and murine I-E molecules, but not to murine I-A molecules in a zinc-dependent fashion. Competition binding studies with other recombinant toxins revealed that SPE-C lacks the generic low affinity major histocompatibility complex (MHC) class II α-chain binding site common to all other bacterial superantigens. Despite this, SPE-C cross-links MHC class II to induce homotypic aggregation of class II–bearing B cells. Nondenaturing sodium dodecyl sulfate electrophoresis and size exclusion chromatography revealed that both wild-type and recombinant SPE-C exist in a stable dimer at neutral or alkaline pH. These data support a recent crystal structure of SPE-C and reveal yet another mechanism by which bacterial superantigens ligate and cross-link MHC class II.
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Stypmann, Jörg, Markus A. Engelen, Clemens Troatz, Markus Rothenburger, Lars Eckardt, and Klaus Tiemann. "Echocardiographic assessment of global left ventricular function in mice." Laboratory Animals 43, no. 2 (April 2009): 127–37. http://dx.doi.org/10.1258/la.2007.06001e.

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Doppler-echocardiographic assessment of cardiovascular structure and function in murine models has developed into one of the most commonly used non-invasive techniques during the last decades. Recent technical improvements even expanded the possibilities. In this review, we summarize the current options to assess global left ventricular (LV) function in mice using echocardiographic techniques. In detail, standard techniques as structural and functional assessment of the cardiovascular phenotype using one-dimensional M-mode echocardiography, two-dimensional B-mode echocardiography and spectral Doppler signals from mitral inflow respective aortal outflow are presented. Further pros and contras of recently implemented techniques as three-dimensional echocardiography and strain and strain rate measurements are discussed. Deduced measures of LV function as the myocardial performance index according to Tei, estimation of the mean velocity of circumferential fibre shortening, LV wall stress and different algorithms to estimate the LV mass are described in detail. Last but not least, specific features and limitations of murine echocardiography are presented. Future perspectives in respect to new examination techniques like targeted molecular imaging with advanced ultrasound contrast bubbles or improvement of equipment like new generation matrix transducers for murine echocardiography are discussed.
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Verbeke, Frederick, Nathan Debunne, Yorick Janssens, Bart De Spiegeleer, and Evelien Wynendaele. "A bioanalytical screening method for Enterococcus faecalis RNPP-type quorum sensing peptides in murine feces." Bioanalysis 14, no. 3 (February 2022): 151–67. http://dx.doi.org/10.4155/bio-2021-0225.

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Background: Bacteria coordinate their behavior as a group via communication with their peers, known as ‘quorum sensing’. Enterococcus faecalis employs quorum sensing via RNPP-peptides which were not yet reported to be present in mammalian biofluids. Results: Solid phase extraction of murine feces was performed, followed by ultra high performance liquid chromatography (UHPLC–MS/MS) in multiple reaction monitoring (MRM) mode (in total <90 min/sample) for the nine known RNPP peptides. Limits of detection ranged between 0.045 and 52 nM. Adequate identification criteria allowed detection of RNPP quorum sensing peptides in 2/20 wild-type murine feces samples (i.e., cAM373 and cOB1). Conclusion: A fit-for-purpose UHPLC–MS/MS method detected these RNPP peptides in wild-type murine feces samples.
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Journal articles Dissertations / Theses Books

Dissertations / Theses on the topic "Murine mode":

1

Pileyre, Baptiste. "Etude préclinique évaluant l'utilisation de la fraction vasculaire stromale et les cellules souches dérivées de tissu adipeux dans le traitement des myosites." Electronic Thesis or Diss., Normandie, 2023. http://www.theses.fr/2023NORMR054.

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Les myosites représentent un ensemble de maladies musculaires auto-immunes touchant les muscles squelettiques et conduisant à des atteintes graves. Si la plupart des patients répondent aux traitements conventionnels, certains restent réfractaires. La fraction vasculaire stromale (FVS), fraichement extraite du tissu adipeux, ou les cellules souches en dérivant (ADSC) par culture d’amplification ont montré des résultats prometteurs dans différentes pathologies auto-immunes et pourraient permettre la prise en charge de ces patients. Afin d’évaluer leur potentiel et d’étudier les mécanismes d’action de ces thérapies, nous avons réalisé des études précliniques in vitro et in vivo. Pour cela, nous avons caractérisé et utilisé un modèle murin de myosites, la souris NOD Icos-/-, présentant des atteintes musculaires spontanées associées à des infiltrats leucocytaires importants. Afin de se rapprocher de l’utilisation autologue de ces thérapies, nous avons réalisé des greffes syngéniques de FVS et d’ADSC dans ce modèle. Nous avons pu observer un ralentissement de l’évolution de la symptomatologie, une réduction de la perte de force musculaire ainsi qu’une diminution de l’atrophie musculaire in vivo. Nous avons mis en évidence une meilleure efficacité des ADSC, en particulier lors des tests in vitro. Ces tests réalisés avec des cellules de donneurs, évaluant l’efficacité de la régénération (test de formation de colonies fibroblastiques) et l’effet immunomodulateur (test d’inhibition de la prolifération lymphocytaire), ont permis de démontrer l’effet dose-dépendant de ces thérapies ainsi que la supériorité des ADSC à la fois en termes d’efficacité maximale et de dose inhibitrice de 50% de l’effet immunomodulateur. Ils nous ont aussi permis d’identifier des marqueurs prédictifs des effets prolifératif (CD90, CD105 ou encore le taux élevé de cellules souches hématopoïétiques) et immunomodulateur (CD73 ou le taux de macrophages) de ces thérapies. L’ensemble de ces éléments démontrent le potentiel de ces thérapies dans le traitement des myosites et l’intérêt d’investiguer leur effet au travers d’essais cliniques
Myositis is a group of autoimmune muscular diseases affecting skeletal muscles, leading to severe damage. While most patients respond to conventional treatments, some remain refractory. The stromal vascular fraction (SVF), freshly extracted from adipose tissue, or stem cells derived from it (ADSC) by expansive culture have shown promising results in various autoimmune pathologies and could enable the management of these patients. To assess their potential and study the mechanisms of action of these therapies, we carried out preclinical studies in vitro and in vivo. To this end, we characterized and used a mouse model of myositis, the Icos-/- NOD mouse, showing spontaneous muscle damage associated with extensive leukocyte infiltrates. To be closer of the autologous use of these therapies, we performed syngeneic transplants of FVS and ADSC in this model. We observed a slowdown in the progression of symptoms, a reduction in the loss of muscle strength and a decrease in muscle atrophy in vivo. We have demonstrated a greater efficacy of ADSCs, particularly in in vitro assays. These tests, carried out with donor cells and assessing regenerative efficacy (fibroblast colony forming unit assay) and immunomodulatory effect (lymphocyte proliferation inhibition assay), demonstrated the dose-dependent effect of these therapies, as well as the superiority of ADSCs in terms of both maximum efficacy and 50% inhibitory dose of the immunomodulatory effect. They also enabled us to identify markers predictive of the proliferative (CD90, CD105 or high hematopoietic stem cell count) and immunomodulatory (CD73 or macrophage count) effects of these therapies. All these elements demonstrate the potential of these therapies in the treatment of myositis, and the interest of investigating their effect through clinical trials
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Castelló, Carla Martí. "Ultrassonografia do tumor sólido de Ehrlich inoculado em camundongos." Universidade Federal de Goiás, 2017. http://repositorio.bc.ufg.br/tede/handle/tede/7130.

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The research to prevent cancer, diagnose early, and find new therapies is one of the main challenges of current medicine, and in vivo tumor models are essential for this aim. Imaging techniques, such as ultrasound, assists the research by helping to obtain data that are more accurate and to reduce the number of animals necessary to obtain statistically significant results. Ehrlich carcinoma is one of the most widely used models but it has not an ultrasonographic description. In this study, serial ultrasound examinations were performed, in B-mode and Doppler, on Ehrlich solid carcinomas (ESC) inoculated in mice. From the measurements obtained by ultrasound, the growth patterns were analyzed and the tumors were separated in two groups depending on the specific growth rate (SGR). Ultrasonographic characteristics of capsule, margins, echotexture, vascular flow, and Doppler indices of Resistivity Index (RI) and Pulsability Index (PI) were compared between groups. ESC presents variable growth patterns; a capsule detectable by ultrasound, which sometimes present discontinuity; detectable flow in most of the exams; and the possibility of a central focus of necrosis or several necrosis focuses separated by tissue. In conclusion, tumors with high vascularization tend to have high SGR, while tumors that presented homogeneous echotexture and absence of blood flow tend to have lower SGR. The study also showed that changes in tumor vessels are reflected in Doppler indices, with significantly lower RI and PI, than normal vessels
A pesquisa para o diagnóstico precoce, prevenção e novos tratamentos do câncer é um dos principais desafios da medicina atual e os modelos tumorais in vivo são imprescindíveis para esse fim. Técnicas de imagem, como a ultrassonografia, auxiliam a obter dados mais precisos e diminuir o número de animais para obter resultados estatisticamente significativos. O carcinoma de Ehrlich é um dos modelos mais usados, mas não existem descrições ultrassonográficas dele. Nesse trabalho, foram realizados exames ultrassonográficos seriados, em modo-B e Doppler, em carcinomas sólidos de Ehrlich (ESC) inoculados em camundongos. A partir das medidas obtidas por ultrassom, foram analisados os padrões de crescimento e os tumores foram separados em dois grupos dependendo da taxa específica de crescimento (SGR). Foram comparadas as características ultrassonográficas da capsula, margens, ecotextura, distribuição e quantidade de fluxo e os índices Doppler, Índice de Resistividade (IR) e Índice de Pulsabilidade (IP), entre os grupos. Os ESCs apresentaram-se como tumores com padrões de crescimento variáveis; uma capsula detectável por ultrassonografia, mas que pode apresentar descontinuidade em alguns casos; fluxo detectável na maioria dos exames; e que podem apresentam um foco de necrose central ou vários focos de necrose separados. Conclui-se que os tumores que apresentam alta vascularização tendem a ter alta SGR enquanto os que apresentam ausência de fluxo e ecotextura homogênea estão correlacionados com baixa SGR. O estudo também demonstrou que as alterações e mudanças nos vasos tumorais se encontram refletidas nos índices Doppler, apresentando IR e IP significativamente menores as dos vasos extratumorais.
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Zgheib, Sara. "Altérations physiologiques et récupération à long terme dans un modéle murin de séparation associée à une restriction du temps d'accés à l'alimentation : un outil pour l'étude des conséquences de l'anorexie mentale." Thesis, Littoral, 2014. http://www.theses.fr/2014DUNK0428/document.

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L'anorexie mentale (AM) est un trouble du comportement alimentaire qui se caractérise par une recherche obsessionnelle de minceur, une forte réduction de la prise alimentaire et une distorsion de l'image de soi. Elle est associée à de multiples perturbations endocriniennes et métaboliques, et à une altération de la masse et de la microarchitecture osseuses. Les facteurs et les mécanismes qui interviennent dans cette maladie sont très mal connus ce qui limite les options thérapeutiques. Il est donc nécessaire de développer un modèle animal qui reproduise les perturbations physiologiques observées en AM et permette d'étudier les facteurs associés à l'altération osseuse. Dans ce but nous avons développé un modèle murin avec une restriction du temps d'accès à l'alimentation associée à un stress induit par la séparation (separation-based anorexia, SBA). Cette phase SBA de 10 semaines est suivie d'une phase de récupération en conditions standard (REC) de 10 semaines. Chez les souris femelles C57B1/6 en fin de croissance rapide, la phase SBA induit une perte rapide et importante du poids corporel. L'analyse de la composition corporelle par DEXA révèle une diminution rapide de près de 40% de la masse grasse ainsi qu'une baisse progressive de la masse maigre et un arrêt de l'acquisition de la masse osseuse. Au niveau des tibias, la densité minérale cortical et la microarchitecture trabéculaire sont altérées. L'observation des frottis vaginaux et la mesure des ovaires révèlent une perturbation importante des fonctions reproductrices. Les tests de tolérance au glucose ont montré que les souris SBA ont une capacité très élevée à corriger la glycémie. Ces animaux sont fortement hypoleptinémiques, et l'axe GH-IGF-1 est très perturbé. L'étude de l'expression génique de différents tissus adipeux a montré une augmentation du niveau des marqueurs de lipogénèse et de lipolyse, ainsi qu'une forte induction du phénotype "adipocyte brun" dans le tissu adipeux sous-cutané. Après deux semaines de REC, les souris SBA retrouvent très rapidement leur poids corporel, leurs masses maigre et grasse. La masse minérale toujours basse à ce stade est corrigée après 10 semaines de REC, ainsi que la microarchitecture osseuse (étude préliminaire). Tous les autres paramètres étudiés sont normalisés, sauf l'hypoleptinémie qui étonnamment persiste même après 10 semaines de protocol REC et malgré la normalisation de la masse adipeuse. D'après ces résultats, on peut conclure que le modèle SBA reproduit de nombreuses perturbations physiologiques observées en AM. La phase de REC révèle que ces souris ont une importante capacité de récupération. L'hypoleptinémie persistante pourrait favoriser la récupération. L'identification des mécanismes impliqués pourrait fournir des pistes thérapeutiques afin de favoriser la reconstitution du capital osseux des patientes anorexiques
Anorexia nervosa (AN) is an eating disorder mainly developed in adolescent girls and young women. It is characterized by an obsessive search for thinness, a profound undernutrition and a distorted self-image.It is associated with multiple endocrine and metabolic disturbances, decreased bone mass and microarchitectural alteration. Some of the developed adaptations are supposed to be involved in the blockade of the pathologic state. Unfortunately, these adaptations are poorly known and most of them cannot be studied on patients. So it is necessary to develop an animal model which mimics the main consequences observed in human pathology and allows studying the recovery process. For this purpose we adapted a murine model of time restricted feeding associated with chronic stress induced by separation-based anorexia (SBA). C57B1/6 female mice are submitted to a long term SBA protocol (10 weeks) and then a long term phase of recovery (10 weeks). At the beginning of the protocol mice are 8 weeks old, so their fast growth is finishing. SBA protocol induced a rapid and significant loss of body weight. Body composition analysis by DEXA showed a 40% decrease of the fat mass, a progressive loss of lean mass and a blockade of bone mass acquisition. Mice deveoped a high glucose tolerance. The observation of vaginal smears revealed a disruption of the estrous cycle and ovarian histology showed an atrophy of the ovaries. These two alterations suggest a major alteration of reproductive functions. These animals showed a very low leptinemia, and the GH/IGF-1 axis was disrupted. The study of bone alteration by microtomography indicated an alteration of bone microarchitecture and of cortical bone mass, mimicking osteoporosis often described in AN patients. Body weight, lean and fat masses were normalized quickly during the REC protocol. Bone mineral content still low after 2 weeks of REC protocol was fully corrected after 10 weeks. The estrous cycle ovarian size and the GH/IGF-I were normalized. Surprisingly, hypoleptinemia persisted even after 10 weeks of REC and despite the normalization of the fat mass. This result has been confirmed by the low level of leptin gene expression in various adipose tissues. Finally, the SBA protocol is valuable model of AN because numerous physiological alterations described in AN are mimicked in this model. The recovery phase revealed the high capacity of mice to normalize the long term alterations. Persitent hypoleptinemia could contribute to the normalization of body composition. However, the balance between central and peripheral effects of the uncorrected hypoleptinemia remains to be determined. This persisting hypoleptinemia could be used for the revision of the therapeutic strategies aiming to correct AN-induced osteoporosis
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Pereira, Beatriz Aparecida Soares. "Patogenicidade e imunogenicidade de isolados clínicos do complexo Paracoccidioides brasiliensis." Botucatu, 2019. http://hdl.handle.net/11449/181206.

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Orientador: Rinaldo Poncio Mendes
Resumo: Introdução. A correlação entre gravidade da paracoccidioidomicose e patogenicidade e imunogenicidade dos fungos causadores tem sido pouco investigada e foi o objetivo deste estudo. Metodologia. As cincos cepas Pb192, Pb234, Pb326, Pb417 e Pb531 foram identificadas pelo seqüenciamento da região Exon 2 da gp43. A patogenicidade foi determinada pelo cálculo da dose letal 50% (DL50%) e pela contagem do número de unidades formadoras de colônias, realizada na sexta semana pós-infecção de camundongos BALB/c. A imunogenicidade foi determinada pela avaliação da resposta imune humoral específica, utilizando-se a reação de imunodifusão dupla em gel de ágar e da imunidade celular, determinada pela concentração das citocinas interleucina -2, interleucina-10, interferon-γ, fator de necrose tumoral – α e do fator de crescimento do endotélio vascular, em tecido pulmonar. Quatro amostras clínicas foram recém-isoladas de pacientes com paracoccidioidomicose, provenientes da Região de Botucatu - os isolados Pb234 e Pb417, de pacientes com a forma crônica moderada; o Pb326 de um caso com a forma aguda grave; e o Pb531, de um caso com a forma crônica grave. As demais cepas Pb192, Pb01 e 8334 foram cedidas pelo laboratório de Moléstias infecciosas. Resultados. As cepas Pb417 e Pb326 agruparam-se às cepas identificadas como P. brasiliensis S1a, a Pb531 às P. brasiliensis S1b e as cepas Pb234 e Pb192 às cepas depositadas como P. restrepiensis (PS3). Os resultados demonstraram correlação direta entre ... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: Introduction. The investigation of paracoccidioidomycosis and pathogenicity and immunogenicity of the provoking fungi has been little investigated and was the objective of this study. Methodology. As strains, Pb192, Pb234, Pb326, Pb417 and Pb531 were included by sequencing the Exon 2 region of gp43. The pathogenicity was determined by calculating the 50% lethal dose (LD50%) and by counting the number of colony forming units performed in the sixth week post-infection of BALB / c mice. Immunogenicity was determined by the humoral immune response, using the agar gel immunodiffusion reaction and the cellular immunity, determined the concentration of cytokines interleukin-2, interleukin-10, interferonγ, tumor necrosis factor - and factor of vascular endothelial growth in lung tissue. Surgical has been associated with patients with paracoccidioidomycosis, derived from the Botucatu - the Pb234 and Pb417; the Pb326 of a case with a severe severe form; and Pb531, of a case with severe chronic form. The other strains Pb192, Pb01 and 8334 were transferred by the laboratory of Infectious Diseases. Results. Pb417 and Pb326 strains were grouped into the associated strains P. brasiliensis S1a, Pb531 to P. brasiliensis S1b and strains Pb234 and Pb192 to strains deposited as P. restrepiensis (PS3). The results demonstrate the pathogenicity of disease error and severity. The small LD 50 values were measured in the following cases: severe disease, Pb531 and Pb326. Pb531 strain was considered to... (Complete abstract click electronic access below)
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Silva, Muriel Vilela Teodoro. "Avaliação do efeito da expressão do gene da interleucina 32 (IL-32) humana em modelo murino de infecção por Leishmania (Leishmania) amazonensis." Universidade Federal de Goiás, 2016. http://repositorio.bc.ufg.br/tede/handle/tede/6333.

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Fundação de Amparo à Pesquisa do Estado de Goiás - FAPEG
IL-32 is a proinflammatory cytokine which has different isoforms. IL-32γ isoform is the most powerful and was detected in lesions of patients with cutaneous leishmaniasis. Murine cells respond to IL-32, however mice lack the gene for this cytokine. To understand the role of IL- 32 in Leishmania (L.) amazonensis, we used transgenic mice for human IL-32γ (IL-32γTg). C57BL/6 mice (WT) and C57BL/6 IL-32γTg were infected with L. amazonensis promastigotes in the ear. The lesion development was followed weekly with a digital caliper (measured in mm of injury). After 3, 6 and 9 weeks, the animals were euthanized for tissue parasitism analysis by the limiting dilution technique, in infected ears, draining lymph node and spleen of mice. The draining lymph node cells were incubated (48 h) in the presence or absence of L. amazonensis antigen (Ag) for analysis of cytokines by ELISA. IL-32γTg mice present IL-32 production in spleen, liver, lymph node and ear. IL-32γTg mice have a lower injury than the WT mice during the third week of infection. From the 5th to the 9th week of infection, the two groups had similar lesion development profiles. Interestingly, in the 3rd week of infection, the parasitic load in the lesion of IL-32γTg mice was 100 times greater than that of WT mice. After three weeks, IL-32γTg mice maintained the same parasitic load up to nine weeks. In WT mice, however, the number of parasites increased exponentially during weeks evaluated. The parasite load in the spleen and lymph node was lower in IL-32γTg mice when compared with WT mice. There was no difference in histological sections of the lesions in WT and IL-32γTg mice infected with L. amazonensis. We did not observe differences between WT and IL-32γTg groups on the product -10) by lymph node cells stimulated with Ag, in the 3rd, 6th and 9th week of infection. Our data suggest that IL-32γ favors infection by L. amazonensis in the early stages, allowing the growth of the parasites. However, this cytokine seems to limit the growth and spread of parasites in the later stages of infection. In vitro analyzes show the similar percentage of infected cells and the number of parasites per infected cell in WT macrophages and IL-32γTg after 3 and 48h of infection with L. amazonensis. However, the production of NO by macrophages seems to be lower in IL- 32γTg mouse cells during infection with L. amazonensis. Understanding the mechanisms by which IL-32γ modulates Leishmania amazonensis infection in mice is essential to define the components that control cutaneous leishmaniasis caused by this specie in humans.
A IL-32 é uma citocina pró-inflamatória que apresenta diferentes isoformas. A isoforma IL- 32γ é a mais potente e foi detectada em lesões de pacientes com leishmaniose tegumentar americana. Células murinas respondem à IL-32, no entanto, camundongos não têm o gene para essa citocina. Para entender o papel da IL-32 na infecção por Leishmania (Leishmania) amazonensis, foram utilizados camundongos transgênicos para a IL-32γ humana (IL-32γTg). Camundongos C57BL/6 (WT) e C57BL/6 IL-32γTg foram infectados com formas promastigotas de L. amazonensis na orelha. O desenvolvimento da lesão foi acompanhado semanalmente com paquímetro digital (medida em mm de lesão). Após 3, 6 e 9 semanas, os animais foram eutanasiados para análise de parasitismo tecidual, pela técnica de diluição limitante, nas orelhas infectadas, no linfonodo drenante e no baço dos camundongos. As células do linfonodo drenante foram incubadas (48 h), na presença ou ausência de antígeno de L. amazonensis (Ag), para análise de citocinas pela técnica de ELISA. Camundongos IL- 32γTg apresentam produção de IL-32 no baço, fígado, linfonodo e orelha. Camundongos IL- 32γTg apresentam uma lesão menor do que a lesão dos camundongos WT, na terceira semana de infecção. Da 5ª até a 9a semana de infecção, os dois grupos apresentaram perfis semelhantes de desenvolvimento da lesão. Curiosamente, na 3ª semana de infecção, a carga parasitária na lesão do camundongo IL-32γTg era 100 vezes maior do que a dos camundongos WT. Após três semanas, os camundongos IL-32γTg mantiveram a mesma carga parasitária até nove semanas. Em camundongos WT, no entanto, o número de parasitos aumentou exponencialmente durante as semanas avaliadas. A carga parasitária do linfonodo e no baço foi menor nos camundongos IL-32γTg, quando comparado com camundongos WT. Não foi observada diferença nos perfis histológicos das lesões nos camundongos WT e IL-32γTg infectados por L. amazonensis. Não foi observada nenhuma diferença entre os grupos WT e IL-32γTg em relação à produção de citocinas (IFNγ, TNFα e IL-10), pelas células dos linfonodos estimuladas com Ag, na 3a, 6a e 9a semana de infecção. Os nossos dados sugerem que a IL-32γ favorece a infecção por L. amazonensis nas fases iniciais, permitindo o crescimento do parasito; no entanto, essa citocina parece limitar o crescimento e a disseminação dos parasitos nas fases mais tardias da infecção. As análises in vitro mostraram porcentagem de células infectadas e número de parasitas por célula infectada semelhantes nos macrófagos dos WT e IL-32γTg com 3 e 48h de infecção por L. amazonensis. Entretanto, a produção de NO por macrófagos parece ser menor nas células de camundongos IL-32γTg durante a infecção por L. amazonensis. Compreender os mecanismos pelos quais a IL-32γ modula a infecção por L. amazonensis nos camundongos é fundamental para a definição dos componentes que controlam a leishmaniose tegumentar causada por esta espécie em seres humanos.
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Zapana, Priscila Rosse Mamani. "Desenvolvimento de um modelo murino para estudo da resposta imune conferida pela proteína do Nucleocapsídeo do vírus Oropouche." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/17/17147/tde-25042018-153023/.

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O vírus Oropouche (OROV) é um arbovírus que ocorre na região amazônica causando surtos de doenças febris agudas e que, ocasionalmente, podem ser associados a meningoencefalite. Aproximadamente 500.000 casos de Oropouche teriam ocorrido no Brasil. Entretanto, não existe vacina contra o OROV. O objetivo deste trabalho foi desenvolver um modelo animal de infecção por OROV para estudar a patogênese da doença e um modelo para testar candidatas vacinais. Protótipo vacinal utilizando a proteína recombinante do nucleocapsídeo (N) de OROV (NrOROV), que é o principal antígeno viral, foi usado como potencial candidato para vacina. Neste estudo utilizou-se um modelo animal em camundongos Balb/c de 12 semanas de idade, inoculados intracerebralmente com 8x105 PFU de OROV, capaz de induzir 100% de letalidade após o terceiro dia da infecção. Altos títulos virais foram encontrados no cérebro e na medula espinhal dos animais. Surpreendentemente, 12 e 24 horas pós-infecção foi possível detectar vírus no fígado e baço (3 Log10 PFU/g) dos camundongos. Com este modelo foram testados os candidatos vacinais. Grupos de camundongos foram imunizados 3 vezes com OROV, OROV e FCA, NrOROV, NrOROV e FCA, NrOROV, Poli I:C e Montanide ISA 720. Após 3 imunizações, os animais foram desafiados com 10 LD50 de OROV e observados por 20 dias. Os animais imunizados com NrOROV e adjuvantes, não foram capazes de produzir anticorpos neutralizantes e adquirir imunidade protetora contra OROV enquanto que os imunizados com OROV apresentaram altos níveis de anticorpos neutralizantes e completa proteção in vivo. Ainda, os anticorpos produzidos pelos animais imunizados permitiram estudar o ciclo de replicação celular do OROV utilizando imunofluorescência.
Oropouche (OROV) is an arbovirus that occurs in the South American, Amazon region, producing outbreaks of acute febrile illness occasionally associated to meningoencephalitis. Approximately 500,000 cases of Oropouche have been reported in Brazil in the last 60 years. However, there is no available vaccine for OROV. We show here the development of an animal model of OROV suitable for studies on pathogenesis and vaccine testing. A vaccine prototype based on recombinant OROV nucleocapsid protein (NrOROV), an important viral antigen, was evaluated in the animal model. Initialy, we observed that all 12-week-old Balb/c mice inoculated intracerebrally with 8x105 PFU died after the third day of infection. Surprisingly, OROV genome was detectable in the liver as early as 12 hours post infection (pi) and in the spleen at 24 hours pi at 3 log10 PFU/g. Besides, high viral titers were found in brain and spinal cord. To test the NrOROV as a vaccine candidate, animals divided in 5 groups were immunized subcutaneously 3 times, two weeks apart with either OROV, OROV and Freud complete Adjuvant (FCA), NrOROV, NrOROV and FCA, NrOROV and Poly I:C and Montanide ISA 720. The experiment also included a group of naïve animals. After the third immunization, the animals were challenged with 10LD50 by intracerebral route and followed for 20 days. The animals immunized with NrOROV and adjuvants developed specific antibodies that were not able to neutralize the virus or confer protective immunity against OROV. Nevertheless, mice immunized with OROV showed high levels of neutralizing and protective antibodies. Despite the discouraging results with NrOROV as a vaccine, the mouse model is suitable to study pathogenesis, and to test other vaccines for OROV.
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DE, PONTI GIADA. "Exploring early therapeutic approaches in a Mucopolysaccharidosis type I (MPS I) mouse model." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2022. http://hdl.handle.net/10281/382061.

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In questo progetto di dottorato, sono stati presi in considerazione alcuni punti cruciali relativi alla malattia Mucopolisaccaridosi di tipo I (MPSI) e ai limiti delle attuali terapie, per migliorarle concentrandosi su approcci in epoca neonatale, a livello di combinazione terapeutiche (HSCT e ERT) e di terapia genica, e su riduzione delle tossicità associate ai regimi di condizionamento. Complessivamente, le problematiche più significative riguardo MPSI rimangono la necessità di un intervento precoce e rapido, l’incompleta correzione della malattia in seguito agli attuali approcci terapeutici e gli effetti collaterali dovuti al regime di precondizionamento. La prima parte del progetto si è concentrata sul testare un approccio terapeutico che combinasse i trattamenti canonici per MPSI. È stata testata l'efficacia della combinazione di HSCT ed ERT nel modello murino di MPSI come intervento neonatale, per valutare i benefici aggiuntivi della terapia enzimatica effettuata in modo continuativo a seguito del trapianto di cellule da donatore. Tre opzioni di trattamento sono state confrontate dalla nascita, considerando la mancante attività enzimatica (IDUA), l’accumulo di GAG e di vacuoli nei principali organi viscerali, la risposta nei confronti di IDUA ricombinante e i miglioramenti di tipo scheletrico e cerebrale. Pertanto, un approccio combinato di HSCT ed ERT nel periodo neonatale potrebbe essere applicato per migliorare alcune manifestazioni cliniche di MPSI, soprattutto evitando danni irreversibili. La seconda parte del progetto di dottorato è stata svolta in collaborazione con TIGET-SR e il Prof. Alessandro Aiuti. Si è concentrato sulla sperimentazione di un approccio di terapia genica neonatale in un modello murino di MPSI, considerando l'importanza di correggere precocemente la malattia. In particolare, abbiamo valutato se questo trattamento terapeutico potesse essere applicato nei neonati MPSI e potesse essere una strategia efficace per superare i principali problemi clinici che permangono dopo il trattamento canonico. Abbiamo valutato l'effetto della terapia genica somministrata nei neonati affetti da MPSI, monitorando i valori di IDUA e VCN nel sangue periferico e considerando infine la mancante attività enzimatica (IDUA), l’accumulo di GAG e di vacuoli nei principali organi viscerali, la risposta nei confronti di IDUA ricombinante e i miglioramenti di tipo scheletrico e cerebrale. Contemporaneamente, abbiamo cercato di ridurre gli effetti collaterali causati dal regime di condizionamento nel contesto delle terapie neonatali per MPSI, come progetto parallelo. L’obiettivo principale è stato trasporre l'applicazione di ADC, molecole congiunte di anticorpo-farmaco, capaci di agire specificatamente sulla cellula, come condizionamento per il trattamento neonatale di MPSI, in cui un intervento precoce è fondamentale. Poiché nessuna delle opzioni testate è stata in grado di indurre un sufficiente attecchimento di cellule del donatore da essere rilevante per il trattamento precoce dell'MPSI, ne abbiamo ricercato le cause, dimostrando la necessità di ulteriori studi prima dell'applicazione degli ADC nel modello studiato, in quelli umanizzati e nei cuccioli di MPSI NSG. Analisi preliminari sono state effettuate relativamente all’aumento dei livelli di citochine dopo CD117-SAP nei topi NSG adulti, confrontandoli agli altri regimi di condizionamento, per valutare una possibile applicazione di ADC con farmaci antinfiammatori prima della terapia precoce nei cuccioli MPSI.
The present PhD project has taken into account critical issues around Mucopolysaccharidosis type I (MPSI) and limitations of current therapies to further improve them, by generally focusing on neonatal therapeutic approaches, both in terms of combined HSCT and ERT and of gene therapy, and on trying to reduce the overall toxicities associated with pre-conditioning settings. Overall, the most important open issues regarding this rare life-threatening disorder are the need for a precocious and rapid intervention, the lack of complete disease correction after current therapeutic approaches and side effects due to pre-conditioning regiment. My PhD project partially focused on testing a combined approach of the current standard-of-cares for treating MPSI. HSCT and ERT combination efficacy was tested in a mouse model of MPSI as neonatal intervention, for evaluating additional benefits of continuous enzyme therapy after transplant of donor’s cells. We compared three treatment options starting from MPSI pups’ birth, considering IDUA deficient activity, GAGs storage and vacuoles in visceral organs, the immune response against the recombinant IDUA and skeletal and CNS ameliorations. Therefore, performing a combined approach of HSCT and ERT in the neonatal period could help improving some hard-to-treat MPSI manifestations. The second part of this PhD project was carried out in collaboration with TIGET-SR and Prof. Alessandro Aiuti. It was focused on testing a neonatal gene therapy approach in a mouse model of MPSI, considering the importance of an early phenotype correction. In particular, we evaluated if this early treatment could be applied in MPSI neonates and could be a successful strategy for overcoming the main clinical issues that still remain after current canonical HSCT treatment. We monitored peripheral blood of treated mice for 8 months in terms of enzymatic activity and VCN, and we evaluated the effect of GT performed in MPSI pups at endpoint, considering IDUA deficient activity, vector copies/genome, GAGs storage and vacuoles in visceral organs, the immune response against the recombinant IDUA and skeletal and CNS ameliorations. The last part of this PhD project was centered on trying to reduce the high morbidity and mortality due to the severe conditioning regimen in the context of neonatal MPSI therapies, as a side project. The main objective was to translate the application of hematopoietic cell–specific antibody-drug conjugates (ADCs) as conditioning for early MPSI treatment, in which a precocious intervention is crucial. Since none of the tested setting was able to induce enough engraftment of donor’s cells to be relevant for MPSI early treatment, we tried to understand what could interfere, but we demonstrated the need for further studies prior to ADCs application in humanised models and in MPSI NSG pups. Preliminary results on increased cytokines levels after CD117-SAP in adult NSG compared to other conditioning settings were performed to evaluate impairment of inflammation and possible ADC application with anti-inflammatory drugs prior to early therapy in MPSI pups.
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Palma, Luana Carneiro. "Doença esteatóica não alcoólica do fígado: comparação das alterações histológicas hepáticas entre modelo murino e pacientes obesos." Centro de Pesquisas Gonçalo Moniz, 2013. https://www.arca.fiocruz.br/handle/icict/7149.

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Submitted by Ana Maria Fiscina Sampaio (fiscina@bahia.fiocruz.br) on 2013-10-15T15:33:27Z No. of bitstreams: 1 Luana Palma. Doença esteatotica...2012.pdf: 6491139 bytes, checksum: 17714fa9ab206495fbf5e1aa05890deb (MD5)
Made available in DSpace on 2013-10-15T15:33:27Z (GMT). No. of bitstreams: 1 Luana Palma. Doença esteatotica...2012.pdf: 6491139 bytes, checksum: 17714fa9ab206495fbf5e1aa05890deb (MD5) Previous issue date: 2013
Universidade Federal da Bahia. Salvador, BA, Brasil / Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil
A Doença Esteatótica Não Alcoólica do Fígado (do inglês Nonalcoholic Fatty Liver Disease – NAFLD) é uma doença crônica hepática de caráter espectral, que vai desde a esteatose simples até a esteato-hepatite não alcoólica. A progressão para cirrose e carcinoma hepatocelular têm sido descrita. A NAFLD apresenta aspectos histológicos semelhantes à doença hepática relacionada ao álcool (esteatose, inflamação lobular, corpúsculos de Mallory e fibrose), mas acomete indivíduos com história negativa de consumo excessivo de álcool. A NAFLD é uma das principais doenças crônicas hepáticas mundiais, e os indivíduos obesos representam a maioria dos casos da doença. Os mecanismos envolvidos na progressão da esteatose para esteato-hepatite não são bem compreendidos. Neste aspecto, modelos murinos da NAFLD têm sido frequentemente utilizados para elucidação destes mecanismos. A maioria dos modelos disponíveis é resultante de modificações genéticas e/ou nutricionais e, em geral, não simulam as alterações metabólicas e histológicas comumente vistas em pacientes com NAFLD. Em nosso grupo, foi proposto um novo modelo de NAFLD. Camundongos C57BL/6 alimentados com dieta rica em gordura (High Fat - HF) demonstraram alterações metabólicas e histológicas sugestivas de NAFLD. O objetivo do presente trabalho foi comparar alterações histológicas hepáticas presentes nestes camundongos com as alterações observadas em pacientes obesos. Amostras de fígados de pacientes obesos e de camundongos alimentados com a dieta HF foram utilizadas. Os tecidos hepáticos foram corados em Hematoxilina & Eosina e Picrossírius Red para avaliação das alterações hepáticas (esteatose, balonização, inflamação, corpúsculos de Mallory-Denk e fibrose). Além disso, foi realizada imunoistoquímica para avaliação da presença de células estrelares ativadas e de células progenitoras hepáticas, células envolvidas na fibrose e no desenvolvimento de carcinoma hepatocelular, respectivamente. Os resultados demonstraram que os fígados de todos os pacientes obesos exibiram esteatose macrovacuolar, balonização hepatocelular, inflamação lobular e fibrose perissinusoidal, o que caracterizou estes pacientes como portadores da NAFLD. As mesmas alterações foram observadas em fígados de camundongos alimentados com a dieta HF. As células estrelares ativadas foram observadas em todos os pacientes obesos, assim como em camundongos de dieta HF. As células progenitoras hepáticas foram observadas na maioria dos pacientes obesos. O fígado de todos os camundongos alimentados com dieta HF exibiram células progenitoras hepáticas. A partir dos dados obtidos, pode-se concluir que fígados de camundongos alimentados com dieta HF exibem alterações histológicas hepáticas similares às observadas em pacientes obesos. Isto abre perspectivas para a utilização do modelo proposto em estudos que busquem elucidar os mecanismos envolvidos na patogênese da NAFLD.
Nonalcoholic Fatty Liver Disease (NAFLD) is a chronic liver disease ranging from simple steatosis to nonalcoholic steatohepatitis. The progression to cirrhosis and hepatocellular carcinoma has been reported. The NAFLD shows histological features similar to alcohol-related liver disease (steatosis, lobular inflammation, fibrosis and Mallory-Denk bodies), but affects individuals with no history of excessive alcohol consumption. The NAFLD is a major chronic hepatic disease in the world, and obese individuals represent the majority of cases of the disease. The mechanisms involved in the progression of steatosis to steatohepatitis are not well understood. In this regard, murine models of NAFLD have been frequently used for elucidation of these mechanisms. Most available models are the result of genetic or nutritional modifications, and generally do not mimic metabolic and histologic changes commonly seen in patients with NAFLD. In our group, we have proposed a new model of NAFLD. Mice fed high fat diet (HF diet) demonstrated metabolic and histological features suggestive of NAFLD. The aim of this study was to compare liver histological alterations present in these mice with the changes observed in obese patients. Samples of livers of obese patients and mice fed HF diet were used. For assessment of liver alterations, such as steatosis, ballooning, inflammation, Mallory- Denk bodies and fibrosis, tissues were stained with hematoxylin & eosin and picrossirius red. In addition, the presence of activated stellate and progenitor liver cells was estimated using immunohistochemistry. The results show that the livers of all obese patients exhibited macrovesicular steatosis, hepatocellular ballooning, perisinusoidal fibrosis, and lobular inflammation, which characterized these patients with NAFLD. Similar changes were observed in livers of mice that fed the HF diet. Activated stellate cells were observed in all obese patients as well as in mice HF. Hepatic progenitor cells were observed in most obese patients. The liver of all animals fed the HF diet exhibited liver progenitor cells. From the data obtained, it can be concluded that livers of mice fed with HF diet exhibit liver abnormalities similar to those observed in obese patients. This opens perspectives for the use of the proposed model in studies that seek to elucidate the mechanisms involved in the pathogenesis of NAFLD.
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Fercoq, Frédéric. "Interactions filaire/poumon dans le modèle murin de filariose Litosomoides sigmodontis." Thesis, Paris, Muséum national d'histoire naturelle, 2017. http://www.theses.fr/2017MNHN0018/document.

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Les filaires sont des nématodes parasites transmis à des vertébrés par des arthropodes hématophages. Les espèces filariennes qui s'installent dans les cavités cœlomiques, les vaisseaux lymphatiques ou des tissus conjonctifs ont leurs stades infestants (ou L3) qui migrent via le système lymphatique après leur inoculation dans la peau. En utilisant le modèle murin avec la filaire Litomosoides sigmodontis dont les adultes résident dans la cavité pleurale, deux phases d'interaction des filaires avec les poumons des souris BALB/c sont décrites 1) lors de la migration des L3 de la peau à la cavité pleurale ; 2) pendant la phase patente de l’infection quand les adultes pondent des microfilaires dans la cavité pleurale. Dans la 1ère phase les L3 rejoignent le système sanguin pulmonaire puis traversent les poumons pour entrer dans la cavité pleurale. Ce passage induit une pathologie aigue transitoire: tout d'abord des hémorragies consécutives à la rupture des capillaires pulmonaires, accompagnées d'une augmentation du nombre de neutrophiles pulmonaires et de la libération transitoire d'IL-1β et des alarmines IL-33 et S100A9 dans la cavité pleurale. Le S100A9 semble faciliter la survie des filaires, soit par un effet anti-inflammatoire soit en facilitant la migration des L3. Les neutrophiles peuvent libérer des NETS en réponse aux L3. Dans les jours suivant l'infection, une réponse régulatrice se met en place dans les poumons, avec le recrutement de macrophages et d'éosinophiles, la production d'IL-4, de CCL2 et d'IL9, ainsi que la baisse d'expression de molécules inflammatoires. La formation des granulomes est également observée dans le tissu pulmonaire. Le passage des L3 induit aussi une inflammation des vaisseaux sanguins pulmonaires chez les souris C57BL/6 seulement. Lors de la phase patente de l'infection, 40% des souris ne développent pas de microfilarémie sanguine. La comparaison des réponses des souris microfilarienne et amicrofilarienne montre une exacerbation de l'inflammation pleurale induite par les microfilaires. De plus, les souris microfilarémiques développent une pathologie pulmonaire dépendant des microfilaires consistant en la fibrose de la plèvre viscérale, une accumulation périvasculaire de macrophages et une inflammation bronchoalvéolaire (production de mucus et éosinophilie). Le contrôle des filaires (adultes et microfilaires), mais aussi la mise en place de la pathologie sont dépendantes de l'IL-5 et de l'IL-4R
Filariae are parasitic nematodes transmited to vertebrates by haematophagous arthropods. The filarial species that settle in the coelomic cavities, the lymphatic vessels or the connective tissues have their infectious stages (or L3) which migrate via the lymphatic system after their inoculation into the skin. Using the murine model with the filaria Litomosoides sigmodontis, whose adults reside in the pleural cavity, two phases of interaction between filariae and the lung of BALB/c mice are described 1) during the L3 migration from the skin to the pleural cavity ; 2) during the patent phase of infection, when adults realease microfilariae in the pleural cavity. During the 1st phase L3 join the pulmonary blood system and then cross through the lungs to enter the pleural cavity. This passage induces a transient acute pathology: first haemorrhages following the rupture of the pulmonary capillaries, together with an increase in the number of pulmonary neutrophils and the transient release of IL-1β and the alarmins IL-33 and S100A9 in the pleural cavity. S100A9 appears to facilitate the survival of the filariae either by an anti-inflammatory effect or by facilitating the migration of L3. Neutrophils can release NETs in response to L3. Within days following the infection, a regulatory response takes place in the lungs, with recruitment of macrophages and eosinophils, production of IL-4, CCL2 and IL-9, and downregulation of inflammatory molecules. The formation of granulomas is also observed in pulmonary tissue. The passage of L3 also induces an inflammation of pulmonary blood vessels, in C57BL/6 mice only. During the patent phase of the infection, 40% of the mice do not develop blood microfilaraemia. Comparison of responses of microfilaremic and amicrofilaremic mice shows an exacerbation of pleural inflammation induced by microfilariae. In addition, microfilaremic mice develop microfilaria-dependent pulmonary pathology consisting on fibrosis of the visceral pleura, perivascular accumulation of macrophages and bronchoalveolar inflammation (mucus production and eosinophilia). The control of the filariae (adults and microfilariae), but also the establishment of the pathology are dependent on IL-5 and IL-4R
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Babaie, Yasmin. "A murine model for haemangioblast transplantation." Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/23691.

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A promoter trap strategy was used to target a single allele of the flk-1 gene with one of two reporter constructs. One placed the EGFP reporter under flk-1 transcriptional control, while the other transcribed the selectable HPRT enzyme, which could be used to isolate flk-1 expressing cells in the HM1 hprt deficient ES cell line. Homologous recombination was successfully achieved with both targeting vectors. HPRT targeted selectable lines were successfully isolated. All lines showed appropriate transgene expression at high enough levels for effective HAT selection to isolate pure populations of flk-1 expressing cells. Two methods of deriving haemangioblastic progenitors from ES cells were tested for their efficacy of the isolation of a pure haemangioblast population based on the expression of flk-1. Methylcellulose cultures were found to be highly variable and problematic to carry out successfully whereas monolayer differentiation on collagen IV was more consistent. This system was then used to optimise the differentiation and selection regime applied to the flk-1/HPRT targeted cells in an attempt to isolate a pure haemangioblast progenitor population. Flk-1/HPRT targeted cells were marked with a constitutive GFP transgene, differentiated and selected for flk-1/HPRT expression on collagen IV. The selected cells were injected into the blastocyst stage embryo to see whether a developmentally more advanced cell population would survive and contribute to the expected cell lineages. Contribution of the GFP marked cells was observed in mesodermal and highly vascularised organs such as the heart, liver and kidney but was absent from the ectodermally derived brain. Expression was strongly localised around regions of vacularisation.
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Books on the topic "Murine mode":

1

Gisby, Angela Suzanne (nee Beale). Studies on Chlamydia trachomatis infection in an experimental murine model. Birmingham: University of Birmingham, 1996.

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Abecassis, Michael. The effect of prostaglandins on a murine model of fulminant viral hepatitis. Ottawa: National Library of Canada, 1990.

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Orrell, Julian Maxwell. Genetic influences on the granulatomous inflammatory response in a murine model of tuberculosis. Manchester: University of Manchester, 1994.

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Walker, Mark David. Promotion of accelerated repair in a radiation impaired wound healing model in murine skin. [s.l: The Author], 1999.

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Price, Jessica Caughman. Notch3 Signaling Promotes Adhesion and Tumor Progression in a Murine Epithelial Ovarian Cancer Model. [New York, N.Y.?]: [publisher not identified], 2017.

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Hodgson, Christopher Martin. Production of Interferon-gamma in a murine model of the induction phase of chemical allergy. [s.l.]: typescript, 1997.

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Joshi, Mital. Development and characterization of a graded, in vivo, compressive, murine model of spinal cord injury. Ottawa: National Library of Canada, 2000.

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Kyōto Kōgei Sen'i Daigaku. Bijutsu Kōgei Shiryōkan. Murano Tōgo no jūtaku dezain: Zumen shiryō ni miru sono sekai. 8th ed. Tōkyō: Kokusho Kankōkai, 2015.

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Jones, Christopher David. The development of a murine model for analyzing the Th-cell response to a bovine rotavirus. [s.l.]: typescript, 1993.

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Abdel-Gawad, Yehia Mohamed. Nuclear protein changes in a murine model of myocarditis: The down regulation of histone H1ps, a differentiation - dependent protein. Ottawa: National Library of Canada, 1993.

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Book chapters on the topic "Murine mode":

1

Nishisaka, Nobuyasu, Philo Morse, Richard F. Jones, Ching Y. Wang, and Gabriel P. Haas. "Murine Animal Model." In Renal Cancer, 255–64. Totowa, NJ: Humana Press, 2001. http://dx.doi.org/10.1385/1-59259-144-2:255.

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Feng, Ningguo, Manuel A. Franco, and Harry B. Greenberg. "Murine Model of Rotavirus Infection." In Advances in Experimental Medicine and Biology, 233–40. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1828-4_35.

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Krishnamurthy, Prasanna, Suresh Kumar Verma, and Raj Kishore. "Murine Bone Marrow Transplantation Model." In Manual of Research Techniques in Cardiovascular Medicine, 146–48. Oxford, UK: John Wiley & Sons, Ltd, 2013. http://dx.doi.org/10.1002/9781118495148.ch17.

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Medina, Eva. "Murine Model of Pneumococcal Pneumonia." In Methods in Molecular Biology, 405–10. Totowa, NJ: Humana Press, 2006. http://dx.doi.org/10.1007/978-1-60761-058-8_22.

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Lugade, Amit A., Paul N. Bogner, and Yasmin Thanavala. "Murine Model of Chronic Respiratory Inflammation." In Crossroads between Innate and Adaptive Immunity III, 125–41. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-5632-3_11.

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Little, J. R., S. H. Stein, and K. D. Little. "Amphotericin B — A Model Murine Immunostimulant." In Antibiosis and Host Immunity, 253–63. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-1901-6_29.

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Quan, D., Z. Zhang, A. Jevnikar, R. Zhong, and D. Grant. "Intestinal Transplantation in the Murine Model." In Organtransplantation in Rats and Mice, 649–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72140-3_66.

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Badi, Niharika, and Zobeida Cruz-Monserrate. "Murine Model of Obesity-Induced Cancer." In Methods in Molecular Biology, 195–201. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2014-4_14.

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Wong, Paul K. Y., William S. Lynn, Y. C. Lin, Wonkyu Choe, and P. H. Yuen. "ts1 MoMuLV: A Murine Model of Neuroimmunodegeneration." In Neuroimmunodegeneration, 75–93. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-12579-3_4.

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Charbonnier, Louis-Marie, and Alain Moine. "Rapamycin as Immunosuppressant in Murine Transplantation Model." In Methods in Molecular Biology, 435–45. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-430-8_28.

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Conference papers on the topic "Murine mode":

1

Samatham, Ravikant, and Steven L. Jacques. "Determine scattering coefficient and anisotropy of scattering of murine tissues using reflectance-mode confocal microscopy." In SPIE BiOS, edited by Adam P. Wax and Vadim Backman. SPIE, 2013. http://dx.doi.org/10.1117/12.2005072.

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Moffat, E. H., R. H. Furlong, A. L. Bloom, and J. C. Giddings. "A MURINE MODEL FOR FACTOR VIII ANTIBODY ANTI-IDIOTYPE REAGENTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644030.

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The regulation of factor VIII antibody (FVIIIAb) production in haemophilic and non-haemophilic patients may be effected by anti-idiotype (Aid) antibodies which specifically react with FVIIIAb. Aid antibodies (reagents) were prepared from rabbits immunised with murine monoclonal FVIIIAb. Immuno fluorescent microscopy and cell culture studies were performed using murine hybridoma cells which secreted the FVIIIAbs.Immuno fluorescence studies examined the ability of the Aid reagents to bind to acetone fixed FVIIIAb secreting hybridoma cells. Positive surface membrane and intra-cytoplasmic staining patterns were seen with the Aid reagent when incubated with the corresponding murine hybridoma cell line. This reaction was blocked subsequent to the addition of the corresponding monoclonal FVIIIAb but was preserved when unrelated monoclonal FVIIIAb was incubated with the hybridoma cells. No fluorescence was observed when Aid reagent was incubated with unrelated FVIIIAb secreting hybridoma cultures.Following the addition of Aid reagent to FVIIIAb secreting hybridoma cultures and incubation for 19 hours, the resultant hybridoma supernatants were examined for FVIIIAb content using an immunoradiometric technique. The Aid reagent failed to inhibit FVIIIAb secretion by hybridoma cells. Thus, although Aid reagents were capable of binding to fixed FVIIIAb secreting cells, they failed to inhibit FVIIIAb secretion from hybridoma cultures. The conjugation of Aid reagent with immunotoxin may however have cytotoxic potential. The murine model provides a method for the study of Aid regulation of FVIIIAb production in haemophilia.
3

Batista, Michael, Hadi T. Nia, Karen Cox, Christine Ortiz, Alan J. Grodzinsky, Dick Heinegård, and Lin Han. "Effects of Chondroadherin on Cartilage Nanostructure and Biomechanics via Murine Model." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14516.

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While small leucine rich proteins/proteoglycans (SLRPs) are present in very low concentrations in the extracellular matrix (ECM), they have been shown to be critical determinants of the proper ECM assembly and function in connective tissues [1] including bone [2], cornea [3], and cartilage [4]. However, their direct and indirect roles in matrix biomechanics and the potential for osteoarthritis-related dysfunction of cartilage remain unclear. With the advent of new high resolution nanotechnological tools, the direct quantification of cartilage biomechanical properties using murine models can provide important insights into how secondary ECM molecules, such as SLRPs, affect the function and pathology of cartilage [5]. Previous nanoindentation studies of murine cartilage have assessed the effects of maturation and osteoarthritis-like degradation of cartilage on its biomechanical properties [6, 7]. Recently, murine models have received increased attention because of the availability of specific gene-knockout and gene alteration technologies [8]. For example, chondroadherin (CHAD) is a non-collagenous small leucine-rich proteoglycan (SLRP) with α-helix and β-sheet secondary structure, spatially localized in the territorial matrix (MW = 38 kDa) [9]. In articular cartilage, CHAD is distributed non-uniformly with depth [10], and binds to type II collagen and the α2β1 integrin and is hypothesized to function in the communication between chondrocytes and their surrounding matrix, as well as in the regulation of collagen fibril assembly [11, 12] (Fig. 1). The objective of the present study is to explore the role of CHAD and its depletion on the structure and nanomechanical properties of both superficial and middle/deep zone cartilage. The current methods thereby enabled depth-dependent analysis of cartilage nanostructure and dynamic energy-dissipative mechanisms.
4

Ballesteros-Zebadúa, P., J. M. Lárraga-Gutierrez, O. A. García-Garduño, M. C. Rubio-Osornio, V. Custodio-Ramírez, S. Moreno-Jimenez, J. E. Suarez-Campos, et al. "Irradiation Design for an Experimental Murine Model." In ELEVENTH MEXICAN SYMPOSIUM ON MEDICAL PHYSICS. AIP, 2010. http://dx.doi.org/10.1063/1.3531598.

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Kohn, A., M. Herriges, P. Basak, M. Ma, J. Le Suer, B. R. Thapa, D. N. Kotton, and F. J. Hawkins. "Preclinical Murine Model for Airway Cell Transplantation." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a2547.

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Deka, C., B. E. Lehnert, N. M. Lehnert, G. M. Jones, L. A. Sklar, and J. A. Steinkamp. "Rapid Analysis of Fluorescence Quenching of FITC Conjugated Antibodies on Individual Cells by Phase-Sensitive Flow Cytometry." In Biomedical Optical Spectroscopy and Diagnostics. Washington, D.C.: Optica Publishing Group, 2006. http://dx.doi.org/10.1364/bosd.1996.ca1.

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We demonstrate a high speed method to analyze the impact of self-quenching on fluorescence lifetimes in individual cells by phase-sensitive flow cytometry, using a model system consisting of FITC (fluorescein isothiocyanate) labeled antimouse Thy 1.2 antibodies bound to murine thymus cells.
7

Zhang, Lingzhi, Farah Hedjran, Christopher Larson, Min Yan, and Tony Reid. "Abstract B50: A novel immunocompetent murine model for replicating oncolytic adenoviral therapy." In Abstracts: AACR Special Conference: The Translational Impact of Model Organisms in Cancer; November 5-8, 2013; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1557-3125.modorg-b50.

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Ramella-Roman, Jessica C., Mala Mahendroo, Clothilde Raoux, Gaël Latour, and Marie-Claire Schanne-Klein. "Polarization-resolved Second Harmonic Generation quantification of the uterine cervix remodeling process." In Microscopy Histopathology and Analytics. Washington, D.C.: Optica Publishing Group, 2024. http://dx.doi.org/10.1364/microscopy.2024.mw3a.3.

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We have utilized Polarization Resolved Second Harmonic Generation to image the remodeling uterine cervix in a murine model. We have developed a fully automatic and unbiased process to quantify collagen remodeling at the pixel level (420 nm). We observe a distinct change in collagen fiber arrangement between days 12 and 15 of pregnancy.
9

Riscili, BP, T. Karsies, S. McMaken, D. Dakhlallah, N. Ali, M. Hunter, and CB Marsh. "Micro-RNA Expression in a Murine Model of Sepsis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1165.

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Van Rheen, ZJ, SM Majka, J. West, and E. Nozik-Grayck. "Novel Murine Model To Study Pulmonary Hypertension: Bleomycin + Hypoxia." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1797.

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Reports on the topic "Murine mode":

1

Cook, Alonzo D. Realistic Murine Model for Streptozotocin-induced Diabetic Peripheral Neuropathy. Science Repository OÜ, August 2018. http://dx.doi.org/10.31487/j.rgm.2018.02.006.

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Richfield, Eric. A Murine Model of Genetic and Environmental Neurotoxicant Action. Fort Belvoir, VA: Defense Technical Information Center, September 1999. http://dx.doi.org/10.21236/ada374832.

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Richfield, Eric K. A Murine Model of Genetic and Environmental Neurotoxicant Action. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada415995.

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Richfield, Eric K. A Murine Model of Genetic and Environmental Neurotoxicant Action. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada416202.

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Shannon, Kevin M. Therapeutic and Biologic Studies in a Murine Model of NF1. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada400468.

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Shannon, Kevin. Therapeutic and Biologic Studies in a Murine Model of NF1. Fort Belvoir, VA: Defense Technical Information Center, October 1999. http://dx.doi.org/10.21236/ada391081.

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Shannon, Kevin. Therapeutic and Biologic Studies in a Murine Model of NF1. Fort Belvoir, VA: Defense Technical Information Center, October 2000. http://dx.doi.org/10.21236/ada392385.

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O'Donnell, Christopher P. Sleep Resilience, Comorbid Anxiety, and Treatment in a Murine Model of PTSD. Fort Belvoir, VA: Defense Technical Information Center, April 2014. http://dx.doi.org/10.21236/ada603152.

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Shlomchik, Warren D. Mechanisms of Graft-vs.-Leukemia Against a Novel Murine Model of Chronic Myelogenous Leukemia. Fort Belvoir, VA: Defense Technical Information Center, July 2005. http://dx.doi.org/10.21236/ada443726.

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Jiao, Jing. Molecular Mechanism of Nkx3.1 Deregulation and Its Function in Murine Pten Prostate Cancer Model. Fort Belvoir, VA: Defense Technical Information Center, September 2005. http://dx.doi.org/10.21236/ada446368.

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