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Your search keyword '"Miranda, Aline S."' showing total 4 results
Start Over Author "Miranda, Aline S." Publisher elsevier
4 results on '"Miranda, Aline S."'

1. List of Contributors

Author

Aigner, Bernhard, primary, Allison, W. Ted, additional, Andreatini, Roberto, additional, Antonelli, Marta, additional, Arndt, Saskia S., additional, Austin, Amazon, additional, Brand, Cristin, additional, Bukowska, Joanna, additional, Caprariello, Andrew C., additional, Carlisle, Rachel E., additional, Chaible, Lucas M., additional, Chen, Li, additional, Chen, Mengqi, additional, Chi, Thomas, additional, Choudhury, Mohammed E., additional, Clarke, Iain J., additional, Coleman, Kristine, additional, Colpo, Gabriela D., additional, Damm, Oliver S., additional, Davis, Catherine M., additional, Davis, Erica E., additional, de Lecea, Luis, additional, de Miranda, Aline S., additional, de Souza, Diogo B., additional, Dickhout, Jeffrey G., additional, Donaldson, Paul J., additional, Donnan, Geoffrey A., additional, Emoto, Yuko, additional, Feifel, David, additional, Finzi Corat, Marcus A., additional, Frasch, Martin G., additional, Fukumura, Ryutaro, additional, Fukusato, Toshio, additional, Fuller-Jackson, John-Paul, additional, Fyffe-Maricich, Sharyl, additional, Gawronska-Kozak, Barbara, additional, Getz, Godfrey S., additional, Gondo, Yoichi, additional, Henry, Belinda A., additional, Howells, David W., additional, Jamwal, Sumit, additional, Kasahara, Jiro, additional, Katsanis, Nicholas, additional, Kemp, Matthew W., additional, Kessler, Barbara, additional, Khan, Imran, additional, King, Aileen, additional, Kinoshita, Denise, additional, Klymiuk, Nikolai, additional, Koyama, Ryuta, additional, Kretzschmar, Doris, additional, Kumar, Puneet, additional, Kuncova, Jitka, additional, Kuro, Maki, additional, Kurome, Mayuko, additional, Lardelli, Michael, additional, Lawson, Heather A., additional, Lewejohann, Lars, additional, Lim, Julie C., additional, Lyons, David M., additional, Macleod, Malcolm R., additional, Makino, Shigeru, additional, Martinez-Lage, Marta, additional, Martis, Renita M., additional, Meijer, Ellen, additional, Metz, Gerlinde A.S., additional, Miller, Robert H., additional, Miura, Yuichiro, additional, Mohammed-Ali, Zahraa, additional, Musk, Gabrielle C., additional, Nademi, Samera, additional, Nalca, Aysegul, additional, Newman, Morgan, additional, Nie, Yu, additional, Nishikawa, Noriko, additional, Nomoto, Masahiro, additional, Nordquist, Rebecca E., additional, O’Collins, Victoria E., additional, Ogawa, Masatoshi, additional, Pereira-Sampaio, Marco A., additional, Praud, Jean-Paul, additional, Quevedo, João, additional, Reardon, Catherine A., additional, Regan, Christopher P., additional, Renner, Simone, additional, Ribeiro, Fabiola M., additional, Rocha, Natalia P., additional, Rodriguez-Perales, Sandra, additional, Ruiz, Sara I., additional, Saito, Masatoshi, additional, J.B. Sampaio, Francisco, additional, Schapiro, Steven J., additional, Schatzberg, Alan F., additional, Schulkin, Jay, additional, Shamchuk, Angela L., additional, Shannon, Richard P., additional, Shen, You-Tang, additional, Shilling, Paul D., additional, Stengl, Milan, additional, Stoller, Marshall L., additional, Stürzenbaum, Stephen R., additional, Sviglerova, Jitka, additional, Taguchi, Kazumi, additional, Takahashi, Yoshihisa, additional, Tanabe, Akie, additional, Tanaka, Junya, additional, Tannenbaum, Jerrold, additional, Teixeira, Antônio L., additional, Testani, Jeffrey M., additional, Tierney, Keith B., additional, Torres-Ruiz, Raul, additional, Tsubura, Airo, additional, Tsuji, Ryosuke, additional, Tzou, David T., additional, Usuda, Haruo, additional, Valvassori, Samira S., additional, van der Staay, Franz J., additional, Varela, Roger B., additional, Verdile, Giuseppe, additional, Vorontsova, Irene, additional, Wayhart, Jessica P., additional, Weed, James L., additional, Welsh, JoEllen, additional, Werler, Steffi, additional, Wistuba, Joachim, additional, Wolf, Eckhard, additional, Wünsch, Annegret, additional, Yamamoto, Toshiyuki, additional, Yokoyama, Hironori, additional, Yoshizawa, Katsuhiko, additional, Zaidan Dagli, Maria L., additional, Zhang, Jennifer Y., additional, Zhou, Yu, additional, and Zumbrun, Elizabeth E., additional

Published
2017
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3. Protective effect of a spider recombinant toxin in a murine model of Huntington's disease.

Author

Joviano-Santos JV, Valadão PAC, Magalhães-Gomes MPS, Fernandes LF, Diniz DM, Machado TCG, Soares KB, Ladeira MS, Miranda AS, Massensini AR, Gomez MV, and Guatimosim C

Subjects
Animals, Disease Models, Animal, Glutamic Acid metabolism, Huntington Disease pathology, Mice, Mice, Transgenic, Muscle, Skeletal drug effects, Muscle, Skeletal pathology, Neurons drug effects, Spinal Cord drug effects, Spinal Cord pathology, Huntington Disease drug therapy, Neuroprotective Agents administration & dosage, Spider Venoms administration & dosage
Abstract

Abnormal calcium influx and glutamatergic excitotoxicity have been extensively associated with neuronal death in Huntington's disease (HD), a genetic movement disorder. Currently, there is no effective treatment for this fatal condition. The neurotoxin Phα1β has demonstrated therapeutic effects as a calcium channel blocker, for example during pain control. However, little is known about its neuroprotective effect in HD. Herein, we investigated if Phα1β is effective in inhibiting neuronal cell death in the BACHD mouse model for HD. We performed intrastriatal injection of Phα1β in WT and BACHD mice. No side effects or unusual behaviors were observed upon Phα1β administration. Using three different motor behavior tests, we observed that injection of the toxin in BACHD mice greatly improved the animals' motor-force as seen in the Wire-hang test, and also the locomotor performance, according to the Open field test. NeuN labeling for mature neuron detection revealed that Phα1β toxin promoted neuronal preservation in the striatum and cortex, when injected locally. Intrastriatal injection of Phα1β was not able to preserve neurons from the spinal cord and also not revert muscle atrophy in BACHD mice. Finally, we observed that Phα1β might, at least in part, exert its protective effect by decreasing L-glutamate, measured in cerebrospinal fluid. Our data provide evidence of a novel neuroprotector effect of Phα1β, paving a path for the development of new approaches to treat HD motor symptoms., (Copyright © 2020. Published by Elsevier Ltd.)

Published
2021
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4. Suppressor of cytokine signaling 2 modulates the immune response profile and development of experimental cerebral malaria.

Author

Brant F, Miranda AS, Esper L, Gualdrón-López M, Cisalpino D, de Souza DDG, Rachid MA, Tanowitz HB, Teixeira MM, Teixeira AL, and Machado FS

Subjects
Animals, Brain metabolism, Brain-Derived Neurotrophic Factor metabolism, Cytokines metabolism, Disease Models, Animal, Female, Malaria, Cerebral metabolism, Malaria, Cerebral parasitology, Malaria, Cerebral therapy, Mice, Mice, Inbred C57BL, Mice, Knockout, Nerve Growth Factors metabolism, Plasmodium berghei isolation & purification, Spleen metabolism, Suppressor of Cytokine Signaling Proteins antagonists & inhibitors, Suppressor of Cytokine Signaling Proteins deficiency, Suppressor of Cytokine Signaling Proteins metabolism, T-Lymphocytes, Regulatory metabolism, Th17 Cells metabolism, Transforming Growth Factor beta metabolism, Malaria, Cerebral immunology, Suppressor of Cytokine Signaling Proteins immunology
Abstract

Plasmodium falciparum infection results in severe malaria in humans, affecting various organs, including the liver, spleen and brain, and resulting in high morbidity and mortality. The Plasmodium berghei ANKA (PbA) infection in mice closely recapitulates many aspects of human cerebral malaria (CM); thus, this model has been used to investigate the pathogenesis of CM. Suppressor of cytokine signaling 2 (SOCS2), an intracellular protein induced by cytokines and hormones, modulates the immune response, neural development, neurogenesis and neurotrophic pathways. However, the role of SOCS2 during CM remains unknown. SOCS2 knockout (SOCS2(-/-)) mice infected with PbA show an initial resistance to infection with reduced parasitemia and production of TNF, TGF-β, IL-12 and IL-17 in the brain. Interestingly, in the late phase of infection, SOCS2(-/-) mice display increased parasitemia and reduced Treg cell infiltration, associated with enhanced levels of Th1 and Th17 cells and related cytokines IL-17, IL-6, and TGF-β in the brain. A significant reduction in protective neurotrophic factors, such as glial cell line-derived neurotrophic factor (GDNF) and brain-derived neurotrophic factor (BDNF), was also observed. Moreover, the molecular alterations in the brain of infected SOCS2(-/-) mice were associated with anxiety-related behaviors and cognition impairment. Mechanistically, these results revealed enhanced nitric oxide (NO) production in PbA-infected SOCS2(-/-) mice, and the inhibition of NO synthesis through l-NAME led to a marked decrease in survival, the disruption of parasitemia control and more pronounced anxiety-like behavior. Treatment with l-NAME also shifted the levels of Th1, Th7 and Treg cells in the brains of infected SOCS2(-/-) mice to the background levels observed in infected WT, with remarkable exception of increased CD8(+)IFN(+) T cells and inflammatory monocytes. These results indicate that SOCS2 plays a dual role during PbA infection, being detrimental in the control of the parasite replication but crucial in the regulation of the immune response and production of neurotrophic factors. Here, we provided strong evidence of a critical relationship between SOCS2 and NO in the orchestration of the immune response and development of CM during PbA infection., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Published
2016
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