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Artigo de periodico
Serotonin synthesis protects the mouse colonic crypt from DNA damage and colorectal tumorigenesis (2019)
Sakita, Juliana Yumi; Bader, Michael ; Santos, Emerson Soares dos ; Garcia, Sérgio Britto ; Minto, Stefânia Bovo ; Alenina, Natalia; Brunaldi, Mariângela Ottoboni ; Carvalho, Milene Cristina de; Vidotto, Thiago ; Gasparotto, Bianca; Martins, Ronaldo Bragança ; Silva Junior, Wilson Araújo da ; Brandão, Marcus Lira ; Leite, Caio A; Cunha, Fernando de Queiroz ; Karsenty, Gerard; Squire, Jeremy Andrew ; Uyemura, Sérgio Akira ; Kannen, Vinicius
Source: The Journal of Pathology. Unidades: FMRP, FFCLRP, FCFRP, FFLCH
Subjects: NEOPLASIAS COLORRETAIS, CARCINOGÊNESE, SEROTONINA
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ABNT
SAKITA, Juliana Yumi et al. Serotonin synthesis protects the mouse colonic crypt from DNA damage and colorectal tumorigenesis. The Journal of Pathology, v. 249, n. 1, p. 102-113, 2019Tradução . . Disponível em: https://doi.org/10.1002/path.5285. Acesso em: 03 nov. 2024.
APA
Sakita, J. Y., Bader, M., Santos, E. S. dos, Garcia, S. B., Minto, S. B., Alenina, N., et al. (2019). Serotonin synthesis protects the mouse colonic crypt from DNA damage and colorectal tumorigenesis. The Journal of Pathology, 249( 1), 102-113. doi:10.1002/path.5285
NLM
Sakita JY, Bader M, Santos ES dos, Garcia SB, Minto SB, Alenina N, Brunaldi MO, Carvalho MC de, Vidotto T, Gasparotto B, Martins RB, Silva Junior WA da, Brandão ML, Leite CA, Cunha F de Q, Karsenty G, Squire JA, Uyemura SA, Kannen V. Serotonin synthesis protects the mouse colonic crypt from DNA damage and colorectal tumorigenesis [Internet]. The Journal of Pathology. 2019 ; 249( 1): 102-113.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1002/path.5285
Vancouver
Sakita JY, Bader M, Santos ES dos, Garcia SB, Minto SB, Alenina N, Brunaldi MO, Carvalho MC de, Vidotto T, Gasparotto B, Martins RB, Silva Junior WA da, Brandão ML, Leite CA, Cunha F de Q, Karsenty G, Squire JA, Uyemura SA, Kannen V. Serotonin synthesis protects the mouse colonic crypt from DNA damage and colorectal tumorigenesis [Internet]. The Journal of Pathology. 2019 ; 249( 1): 102-113.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1002/path.5285
Artigo de periodico
Brain stimulation differentially modulates nociception and inflammation in aversive and non-aversive behavioral conditions (2018)
Bassi, G. S.; Kanashiro, A.; Rodrigues, G. J.; Cunha, Fernando de Queiroz; Coimbra, Norberto Cysne; Ulloa, L.
Source: Neuroscience. Unidade: FMRP
Subjects: INFLAMAÇÃO, DOR, COMPORTAMENTO, CÉREBRO
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ABNT
BASSI, G. S. et al. Brain stimulation differentially modulates nociception and inflammation in aversive and non-aversive behavioral conditions. Neuroscience, v. 383, p. 191-204, 2018Tradução . . Disponível em: https://doi.org/10.1016/j.neuroscience.2018.05.008. Acesso em: 03 nov. 2024.
APA
Bassi, G. S., Kanashiro, A., Rodrigues, G. J., Cunha, F. de Q., Coimbra, N. C., & Ulloa, L. (2018). Brain stimulation differentially modulates nociception and inflammation in aversive and non-aversive behavioral conditions. Neuroscience, 383, 191-204. doi:10.1016/j.neuroscience.2018.05.008
NLM
Bassi GS, Kanashiro A, Rodrigues GJ, Cunha F de Q, Coimbra NC, Ulloa L. Brain stimulation differentially modulates nociception and inflammation in aversive and non-aversive behavioral conditions [Internet]. Neuroscience. 2018 ; 383 191-204.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1016/j.neuroscience.2018.05.008
Vancouver
Bassi GS, Kanashiro A, Rodrigues GJ, Cunha F de Q, Coimbra NC, Ulloa L. Brain stimulation differentially modulates nociception and inflammation in aversive and non-aversive behavioral conditions [Internet]. Neuroscience. 2018 ; 383 191-204.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1016/j.neuroscience.2018.05.008
Artigo de periodico
The citrus flavanone naringenin reduces gout-induced joint pain and inflammation in mice by inhibiting the activation of NFκB and macrophage release of IL-1β (2018)
Ruiz-Miyazawa, Kenji W.; Borghi, Sergio M.; Ribeiro, Felipe A. Pinho; Ferrari, Larissa Staurengo; Fattori, Victor; Fernandes, Glaura S. A.; Casella, Antonio M.; Alves Filho, José Carlos Farias ; Cunha, Thiago Mattar ; Cunha, Fernando de Queiroz ; Casagrande, Rubia; Verri, Waldiceu A.
Source: Journal of Functional Foods. Unidade: FMRP
Subjects: ARTRITE, DOR, INFLAMAÇÃO, RATOS, MACRÓFAGOS
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ABNT
RUIZ-MIYAZAWA, Kenji W. et al. The citrus flavanone naringenin reduces gout-induced joint pain and inflammation in mice by inhibiting the activation of NFκB and macrophage release of IL-1β. Journal of Functional Foods, v. 48, p. 106-116, 2018Tradução . . Disponível em: https://doi.org/10.1016/j.jff.2018.06.025. Acesso em: 03 nov. 2024.
APA
Ruiz-Miyazawa, K. W., Borghi, S. M., Ribeiro, F. A. P., Ferrari, L. S., Fattori, V., Fernandes, G. S. A., et al. (2018). The citrus flavanone naringenin reduces gout-induced joint pain and inflammation in mice by inhibiting the activation of NFκB and macrophage release of IL-1β. Journal of Functional Foods, 48, 106-116. doi:10.1016/j.jff.2018.06.025
NLM
Ruiz-Miyazawa KW, Borghi SM, Ribeiro FAP, Ferrari LS, Fattori V, Fernandes GSA, Casella AM, Alves Filho JCF, Cunha TM, Cunha F de Q, Casagrande R, Verri WA. The citrus flavanone naringenin reduces gout-induced joint pain and inflammation in mice by inhibiting the activation of NFκB and macrophage release of IL-1β [Internet]. Journal of Functional Foods. 2018 ; 48 106-116.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1016/j.jff.2018.06.025
Vancouver
Ruiz-Miyazawa KW, Borghi SM, Ribeiro FAP, Ferrari LS, Fattori V, Fernandes GSA, Casella AM, Alves Filho JCF, Cunha TM, Cunha F de Q, Casagrande R, Verri WA. The citrus flavanone naringenin reduces gout-induced joint pain and inflammation in mice by inhibiting the activation of NFκB and macrophage release of IL-1β [Internet]. Journal of Functional Foods. 2018 ; 48 106-116.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1016/j.jff.2018.06.025
Artigo de periodico
15d-PGJ2-loaded nanocapsules ameliorate experimental gout arthritis by reducing pain and inflammation in a PPAR-gamma-sensitive manner in mice (2018)
Ruiz-Miyazawa, Kenji W; Staurengo-Ferrari, Larissa; Pinho-Ribeiro, Felipe A; Fattori, Victor ; Zaninelli, Tiago H ; Badaro-Garcia, Stephanie; Borghi, Sergio M; Andrade, Ketlem C; Clemente-Napimoga, Juliana T; Alves Filho, José Carlos Farias ; Cunha, Thiago Mattar ; Fraceto, Leonardo F; Cunha, Fernando de Queiroz ; Napimoga, Marcelo H ; Casagrande, Rúbia ; Verri Júnior, Waldiceu Aparecido
Source: Scientific Reports. Unidade: FMRP
Subjects: ARTRITE, INFLAMAÇÃO, DOR, RATOS
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ABNT
RUIZ-MIYAZAWA, Kenji W et al. 15d-PGJ2-loaded nanocapsules ameliorate experimental gout arthritis by reducing pain and inflammation in a PPAR-gamma-sensitive manner in mice. Scientific Reports, v. 8, 2018Tradução . . Disponível em: https://doi.org/10.1038/s41598-018-32334-0. Acesso em: 03 nov. 2024.
APA
Ruiz-Miyazawa, K. W., Staurengo-Ferrari, L., Pinho-Ribeiro, F. A., Fattori, V., Zaninelli, T. H., Badaro-Garcia, S., et al. (2018). 15d-PGJ2-loaded nanocapsules ameliorate experimental gout arthritis by reducing pain and inflammation in a PPAR-gamma-sensitive manner in mice. Scientific Reports, 8. doi:10.1038/s41598-018-32334-0
NLM
Ruiz-Miyazawa KW, Staurengo-Ferrari L, Pinho-Ribeiro FA, Fattori V, Zaninelli TH, Badaro-Garcia S, Borghi SM, Andrade KC, Clemente-Napimoga JT, Alves Filho JCF, Cunha TM, Fraceto LF, Cunha F de Q, Napimoga MH, Casagrande R, Verri Júnior WA. 15d-PGJ2-loaded nanocapsules ameliorate experimental gout arthritis by reducing pain and inflammation in a PPAR-gamma-sensitive manner in mice [Internet]. Scientific Reports. 2018 ; 8[citado 2024 nov. 03 ] Available from: https://doi.org/10.1038/s41598-018-32334-0
Vancouver
Ruiz-Miyazawa KW, Staurengo-Ferrari L, Pinho-Ribeiro FA, Fattori V, Zaninelli TH, Badaro-Garcia S, Borghi SM, Andrade KC, Clemente-Napimoga JT, Alves Filho JCF, Cunha TM, Fraceto LF, Cunha F de Q, Napimoga MH, Casagrande R, Verri Júnior WA. 15d-PGJ2-loaded nanocapsules ameliorate experimental gout arthritis by reducing pain and inflammation in a PPAR-gamma-sensitive manner in mice [Internet]. Scientific Reports. 2018 ; 8[citado 2024 nov. 03 ] Available from: https://doi.org/10.1038/s41598-018-32334-0
Artigo de periodico
Interleukin-33 receptor (ST2) deficiency improves the outcome of staphylococcus aureus-induced septic arthritis (2018)
Staurengo-Ferrari, Larissa; Trevelin, Silvia C.; Fattori, Victor; Nascimento, Daniele C.; Lima, Kalil A. de; Pelayo, Jacinta S.; Figueiredo, Florêncio; Casagrande, Rubia; Fukada, Sandra Yasuyo; Teixeira, Mauro M.; Cunha, Thiago Mattar; Liew, Foo Y.; Oliveira, Rene D.; Louzada Júnior, Paulo; Cunha, Fernando de Queiroz; Alves Filho, José Carlos Farias; Verri, Waldiceu A.
Source: Frontiers in Immunology. Unidades: FCFRP, FMRP
Subjects: MACRÓFAGOS, STAPHYLOCOCCUS, INTERLEUCINAS, ÓXIDO NÍTRICO, ARTRITE
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ABNT
STAURENGO-FERRARI, Larissa et al. Interleukin-33 receptor (ST2) deficiency improves the outcome of staphylococcus aureus-induced septic arthritis. Frontiers in Immunology, v. 9, 2018Tradução . . Disponível em: https://doi.org/10.3389/fimmu.2018.00962. Acesso em: 03 nov. 2024.
APA
Staurengo-Ferrari, L., Trevelin, S. C., Fattori, V., Nascimento, D. C., Lima, K. A. de, Pelayo, J. S., et al. (2018). Interleukin-33 receptor (ST2) deficiency improves the outcome of staphylococcus aureus-induced septic arthritis. Frontiers in Immunology, 9. doi:10.3389/fimmu.2018.00962
NLM
Staurengo-Ferrari L, Trevelin SC, Fattori V, Nascimento DC, Lima KA de, Pelayo JS, Figueiredo F, Casagrande R, Fukada SY, Teixeira MM, Cunha TM, Liew FY, Oliveira RD, Louzada Júnior P, Cunha F de Q, Alves Filho JCF, Verri WA. Interleukin-33 receptor (ST2) deficiency improves the outcome of staphylococcus aureus-induced septic arthritis [Internet]. Frontiers in Immunology. 2018 ; 9[citado 2024 nov. 03 ] Available from: https://doi.org/10.3389/fimmu.2018.00962
Vancouver
Staurengo-Ferrari L, Trevelin SC, Fattori V, Nascimento DC, Lima KA de, Pelayo JS, Figueiredo F, Casagrande R, Fukada SY, Teixeira MM, Cunha TM, Liew FY, Oliveira RD, Louzada Júnior P, Cunha F de Q, Alves Filho JCF, Verri WA. Interleukin-33 receptor (ST2) deficiency improves the outcome of staphylococcus aureus-induced septic arthritis [Internet]. Frontiers in Immunology. 2018 ; 9[citado 2024 nov. 03 ] Available from: https://doi.org/10.3389/fimmu.2018.00962
Artigo de periodico
Galectin-3 aggravates experimental polymicrobial sepsis by impairing neutrophil recruitment to the infectious focus (2018)
Ferreira, Raphael Gomes; Rodrigues, Lilian Cataldi ; Nascimento, Daniele Carvalho Bernardo; Kanashiro, Alexandre ; Melo, Paulo Henrique de; Borges, Vanessa de Fátima; Gozzi, Aline ; Prado, Douglas da Silva ; Borges, Marcos de Carvalho; Ramalho, Fernando Silva ; Stowell, Sean R.; Cummings, Richard D.; Dias-Baruffi, Marcelo ; Cunha, Fernando de Queiroz ; Alves-Filho, José Carlos Farias
Source: Journal of Infection. Unidades: FCFRP, FMRP
Subjects: SEPSE, NEUTRÓFILOS, INFLAMAÇÃO
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ABNT
FERREIRA, Raphael Gomes et al. Galectin-3 aggravates experimental polymicrobial sepsis by impairing neutrophil recruitment to the infectious focus. Journal of Infection, v. 77, n. 5, p. 391-397, 2018Tradução . . Disponível em: https://doi.org/10.1016/j.jinf.2018.06.010. Acesso em: 03 nov. 2024.
APA
Ferreira, R. G., Rodrigues, L. C., Nascimento, D. C. B., Kanashiro, A., Melo, P. H. de, Borges, V. de F., et al. (2018). Galectin-3 aggravates experimental polymicrobial sepsis by impairing neutrophil recruitment to the infectious focus. Journal of Infection, 77( 5), 391-397. doi:10.1016/j.jinf.2018.06.010
NLM
Ferreira RG, Rodrigues LC, Nascimento DCB, Kanashiro A, Melo PH de, Borges V de F, Gozzi A, Prado D da S, Borges M de C, Ramalho FS, Stowell SR, Cummings RD, Dias-Baruffi M, Cunha F de Q, Alves-Filho JCF. Galectin-3 aggravates experimental polymicrobial sepsis by impairing neutrophil recruitment to the infectious focus [Internet]. Journal of Infection. 2018 ; 77( 5): 391-397.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1016/j.jinf.2018.06.010
Vancouver
Ferreira RG, Rodrigues LC, Nascimento DCB, Kanashiro A, Melo PH de, Borges V de F, Gozzi A, Prado D da S, Borges M de C, Ramalho FS, Stowell SR, Cummings RD, Dias-Baruffi M, Cunha F de Q, Alves-Filho JCF. Galectin-3 aggravates experimental polymicrobial sepsis by impairing neutrophil recruitment to the infectious focus [Internet]. Journal of Infection. 2018 ; 77( 5): 391-397.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1016/j.jinf.2018.06.010
Artigo de periodico
The atypical chemokine receptor ACKR2 is protective against sepsis (2018)
Castanheira, Fernanda Vargas e Silva; Borges, Vanessa de Fátima; Sônego, Fabiane; Kanashiro, Alexandre ; Donate, Paula Barbim; Melo, Paulo Henrique de; Pallas, Kenneth; Russo, Remo C.; Amaral, Flávio A.; Teixeira, Mauro M.; Ramalho, Fernando Silva ; Cunha, Thiago Mattar ; Liew, Foo Y.; Alves Filho, José Carlos Farias ; Graham, Gerard J.; Cunha, Fernando de Queiroz
Source: SHOCK. Unidade: FMRP
Subjects: SEPSE, QUIMIOTERAPIA
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ABNT
CASTANHEIRA, Fernanda Vargas e Silva et al. The atypical chemokine receptor ACKR2 is protective against sepsis. SHOCK, v. 49, n. 6, p. 682-689, 2018Tradução . . Disponível em: https://doi.org/10.1097/shk.0000000000000969. Acesso em: 03 nov. 2024.
APA
Castanheira, F. V. e S., Borges, V. de F., Sônego, F., Kanashiro, A., Donate, P. B., Melo, P. H. de, et al. (2018). The atypical chemokine receptor ACKR2 is protective against sepsis. SHOCK, 49( 6), 682-689. doi:10.1097/shk.0000000000000969
NLM
Castanheira FV e S, Borges V de F, Sônego F, Kanashiro A, Donate PB, Melo PH de, Pallas K, Russo RC, Amaral FA, Teixeira MM, Ramalho FS, Cunha TM, Liew FY, Alves Filho JCF, Graham GJ, Cunha F de Q. The atypical chemokine receptor ACKR2 is protective against sepsis [Internet]. SHOCK. 2018 ; 49( 6): 682-689.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1097/shk.0000000000000969
Vancouver
Castanheira FV e S, Borges V de F, Sônego F, Kanashiro A, Donate PB, Melo PH de, Pallas K, Russo RC, Amaral FA, Teixeira MM, Ramalho FS, Cunha TM, Liew FY, Alves Filho JCF, Graham GJ, Cunha F de Q. The atypical chemokine receptor ACKR2 is protective against sepsis [Internet]. SHOCK. 2018 ; 49( 6): 682-689.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1097/shk.0000000000000969
Artigo de periodico
Naringenin mitigates titanium dioxide (TiO2)-induced chronic arthritis in mice: role of oxidative stress, cytokines, and NFκB (2018)
Manchope, Marília F.; Artero, Nayara A.; Fattori, Victor; Mizokami, Sandra S.; Pitol, Dimitrius Leonardo; Issa, João Paulo Mardegan; Fukada, Sandra Yasuyo; Cunha, Thiago Mattar; Alves Filho, José Carlos Farias; Cunha, Fernando de Queiroz; Casagrande, Rubia; Verri Júnior, Waldiceu A.
Source: Inflammation Research. Unidades: FORP, FCFRP, FMRP
Subjects: ARTRITE, ARTROPLASTIA, FLAVONOIDES, DOR, INFLAMAÇÃO
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ABNT
MANCHOPE, Marília F. et al. Naringenin mitigates titanium dioxide (TiO2)-induced chronic arthritis in mice: role of oxidative stress, cytokines, and NFκB. Inflammation Research, v. 67, n. 11-12, p. 997-1012, 2018Tradução . . Disponível em: https://doi.org/10.1007/s00011-018-1195-y. Acesso em: 03 nov. 2024.
APA
Manchope, M. F., Artero, N. A., Fattori, V., Mizokami, S. S., Pitol, D. L., Issa, J. P. M., et al. (2018). Naringenin mitigates titanium dioxide (TiO2)-induced chronic arthritis in mice: role of oxidative stress, cytokines, and NFκB. Inflammation Research, 67( 11-12), 997-1012. doi:10.1007/s00011-018-1195-y
NLM
Manchope MF, Artero NA, Fattori V, Mizokami SS, Pitol DL, Issa JPM, Fukada SY, Cunha TM, Alves Filho JCF, Cunha F de Q, Casagrande R, Verri Júnior WA. Naringenin mitigates titanium dioxide (TiO2)-induced chronic arthritis in mice: role of oxidative stress, cytokines, and NFκB [Internet]. Inflammation Research. 2018 ; 67( 11-12): 997-1012.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1007/s00011-018-1195-y
Vancouver
Manchope MF, Artero NA, Fattori V, Mizokami SS, Pitol DL, Issa JPM, Fukada SY, Cunha TM, Alves Filho JCF, Cunha F de Q, Casagrande R, Verri Júnior WA. Naringenin mitigates titanium dioxide (TiO2)-induced chronic arthritis in mice: role of oxidative stress, cytokines, and NFκB [Internet]. Inflammation Research. 2018 ; 67( 11-12): 997-1012.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1007/s00011-018-1195-y
Artigo de periodico
Paclitaxel reduces tumor growth by reprogramming tumor-associated macrophages to an M1- profile in a TLR4-dependent manner (2018)
Wanderley, Carlos W.; Colon, David F.; Luiz, Joao Paulo Mesquita; Oliveira, Francisco F.; Viacava, Paula R.; Leite, Caio A.; Pereira, Janaina A.; Silva, Camila M.; Silva, Cassia R.; Silva, Rangel L.; Hernandez, Cesar A. Speck; Mota, Jose M.; Alves Filho, José Carlos Farias; Lima-Júnior, Roberto C.; Cunha, Thiago Mattar; Cunha, Fernando de Queiroz
Source: Cancer Research. Unidade: FMRP
Subjects: ANTINEOPLÁSICOS, IMUNOLOGIA CELULAR, NEOPLASIAS, MACRÓFAGOS
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ABNT
WANDERLEY, Carlos W. et al. Paclitaxel reduces tumor growth by reprogramming tumor-associated macrophages to an M1- profile in a TLR4-dependent manner. Cancer Research, v. 78, n. 20, p. 5891-5900, 2018Tradução . . Disponível em: https://doi.org/10.1158/0008-5472.can-17-3480. Acesso em: 03 nov. 2024.
APA
Wanderley, C. W., Colon, D. F., Luiz, J. P. M., Oliveira, F. F., Viacava, P. R., Leite, C. A., et al. (2018). Paclitaxel reduces tumor growth by reprogramming tumor-associated macrophages to an M1- profile in a TLR4-dependent manner. Cancer Research, 78( 20), 5891-5900. doi:10.1158/0008-5472.can-17-3480
NLM
Wanderley CW, Colon DF, Luiz JPM, Oliveira FF, Viacava PR, Leite CA, Pereira JA, Silva CM, Silva CR, Silva RL, Hernandez CAS, Mota JM, Alves Filho JCF, Lima-Júnior RC, Cunha TM, Cunha F de Q. Paclitaxel reduces tumor growth by reprogramming tumor-associated macrophages to an M1- profile in a TLR4-dependent manner [Internet]. Cancer Research. 2018 ; 78( 20): 5891-5900.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1158/0008-5472.can-17-3480
Vancouver
Wanderley CW, Colon DF, Luiz JPM, Oliveira FF, Viacava PR, Leite CA, Pereira JA, Silva CM, Silva CR, Silva RL, Hernandez CAS, Mota JM, Alves Filho JCF, Lima-Júnior RC, Cunha TM, Cunha F de Q. Paclitaxel reduces tumor growth by reprogramming tumor-associated macrophages to an M1- profile in a TLR4-dependent manner [Internet]. Cancer Research. 2018 ; 78( 20): 5891-5900.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1158/0008-5472.can-17-3480
Artigo de periodico
Inhibition of spinal p38 MAPK prevents articular neutrophil infiltration in experimental arthritis via sympathetic activation (2018)
Kanashiro, Alexandre; Franchin, Marcelo; Bassi, Gabriel Shimizu; Santana, Dênis Augusto Reis; Cunha, Thiago Mattar; Cunha, Fernando de Queiroz; Ulloa, Luis; Rodrigues, Gerson Jonathan
Source: Fundamental and Clinical Pharmacology. Unidade: FMRP
Subjects: ARTRITE, RECEPTORES ANDROGÊNICOS, SISTEMA NERVOSO PARASSIMPÁTICO, NEUTRÓFILOS
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ABNT
KANASHIRO, Alexandre et al. Inhibition of spinal p38 MAPK prevents articular neutrophil infiltration in experimental arthritis via sympathetic activation. Fundamental and Clinical Pharmacology, v. 32, n. 2, p. 155-162, 2018Tradução . . Disponível em: https://doi.org/10.1111/fcp.12338. Acesso em: 03 nov. 2024.
APA
Kanashiro, A., Franchin, M., Bassi, G. S., Santana, D. A. R., Cunha, T. M., Cunha, F. de Q., et al. (2018). Inhibition of spinal p38 MAPK prevents articular neutrophil infiltration in experimental arthritis via sympathetic activation. Fundamental and Clinical Pharmacology, 32( 2), 155-162. doi:10.1111/fcp.12338
NLM
Kanashiro A, Franchin M, Bassi GS, Santana DAR, Cunha TM, Cunha F de Q, Ulloa L, Rodrigues GJ. Inhibition of spinal p38 MAPK prevents articular neutrophil infiltration in experimental arthritis via sympathetic activation [Internet]. Fundamental and Clinical Pharmacology. 2018 ; 32( 2): 155-162.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1111/fcp.12338
Vancouver
Kanashiro A, Franchin M, Bassi GS, Santana DAR, Cunha TM, Cunha F de Q, Ulloa L, Rodrigues GJ. Inhibition of spinal p38 MAPK prevents articular neutrophil infiltration in experimental arthritis via sympathetic activation [Internet]. Fundamental and Clinical Pharmacology. 2018 ; 32( 2): 155-162.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1111/fcp.12338
Artigo de periodico
Succinate receptor deficiency attenuates arthritis by reducing dendritic cell traffic and expansion of Th17 cells in the lymph nodes (2018)
Saraiva, André L.; Veras, Flávio P.; Peres, Raphael S.; Talbot, Jhimmy; Lima, Kalil A. de; Luiz, João P.; Carballido, José M.; Cunha, Thiago Mattar; Cunha, Fernando de Queiroz; Ryffel, Bernhard; Alves Filho, José Carlos Farias
Source: The FASEB Journal. Unidade: FMRP
Subjects: DOENÇAS AUTOIMUNES, INFLAMAÇÃO, METABOLISMO
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ABNT
SARAIVA, André L. et al. Succinate receptor deficiency attenuates arthritis by reducing dendritic cell traffic and expansion of Th17 cells in the lymph nodes. The FASEB Journal, v. 32, n. 12, p. 6550-6558, 2018Tradução . . Disponível em: https://doi.org/10.1096/fj.201800285. Acesso em: 03 nov. 2024.
APA
Saraiva, A. L., Veras, F. P., Peres, R. S., Talbot, J., Lima, K. A. de, Luiz, J. P., et al. (2018). Succinate receptor deficiency attenuates arthritis by reducing dendritic cell traffic and expansion of Th17 cells in the lymph nodes. The FASEB Journal, 32( 12), 6550-6558. doi:10.1096/fj.201800285
NLM
Saraiva AL, Veras FP, Peres RS, Talbot J, Lima KA de, Luiz JP, Carballido JM, Cunha TM, Cunha F de Q, Ryffel B, Alves Filho JCF. Succinate receptor deficiency attenuates arthritis by reducing dendritic cell traffic and expansion of Th17 cells in the lymph nodes [Internet]. The FASEB Journal. 2018 ; 32( 12): 6550-6558.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1096/fj.201800285
Vancouver
Saraiva AL, Veras FP, Peres RS, Talbot J, Lima KA de, Luiz JP, Carballido JM, Cunha TM, Cunha F de Q, Ryffel B, Alves Filho JCF. Succinate receptor deficiency attenuates arthritis by reducing dendritic cell traffic and expansion of Th17 cells in the lymph nodes [Internet]. The FASEB Journal. 2018 ; 32( 12): 6550-6558.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1096/fj.201800285
Artigo de periodico
The host control of a clinical isolate strain of P. aeruginosa infection is independent of Nod-1 but depends on MyD88 (2018)
Sônego, Fabiane; Castanheira, Fernanda V. S.; Horta, Catarina V.; Kanashiro, Alexandre; Czaikoski, Paula G.; Zamboni, Dario Simões; Alves Filho, José Carlos Farias; Cunha, Fernando de Queiroz
Source: Inflammation Research. Unidade: FMRP
Subjects: PNEUMONIA, NEUTRÓFILOS, QUIMIOCINAS, BACTÉRIAS GRAM-NEGATIVAS
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
ABNT
SÔNEGO, Fabiane et al. The host control of a clinical isolate strain of P. aeruginosa infection is independent of Nod-1 but depends on MyD88. Inflammation Research, v. 67, n. 5, p. 435-443, 2018Tradução . . Disponível em: https://doi.org/10.1007/s00011-018-1135-x. Acesso em: 03 nov. 2024.
APA
Sônego, F., Castanheira, F. V. S., Horta, C. V., Kanashiro, A., Czaikoski, P. G., Zamboni, D. S., et al. (2018). The host control of a clinical isolate strain of P. aeruginosa infection is independent of Nod-1 but depends on MyD88. Inflammation Research, 67( 5), 435-443. doi:10.1007/s00011-018-1135-x
NLM
Sônego F, Castanheira FVS, Horta CV, Kanashiro A, Czaikoski PG, Zamboni DS, Alves Filho JCF, Cunha F de Q. The host control of a clinical isolate strain of P. aeruginosa infection is independent of Nod-1 but depends on MyD88 [Internet]. Inflammation Research. 2018 ; 67( 5): 435-443.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1007/s00011-018-1135-x
Vancouver
Sônego F, Castanheira FVS, Horta CV, Kanashiro A, Czaikoski PG, Zamboni DS, Alves Filho JCF, Cunha F de Q. The host control of a clinical isolate strain of P. aeruginosa infection is independent of Nod-1 but depends on MyD88 [Internet]. Inflammation Research. 2018 ; 67( 5): 435-443.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1007/s00011-018-1135-x
Artigo de periodico
Smoking-induced aggravation of experimental arthritis is dependent of aryl hydrocarbon receptor activation in Th17 cells (2018)
Talbot, Jhimmy; Peres, Raphael S.; Pinto, Larissa G.; Oliveira, Rene D. R.; Lima, Kalil A.; Donate, Paula B.; Silva, Jaqueline R.; Ryffel, Bernard; Cunha, Thiago Mattar; Alves Filho, José Carlos Farias; Liew, Foo Y.; Louzada Júnior, Paulo; Cunha, Fernando de Queiroz
Source: Arthritis Research & Therapy. Unidade: FMRP
Subjects: ARTRITE REUMATOIDE, FUMANTES, INFLAMAÇÃO, HIDROCARBONETOS
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
ABNT
TALBOT, Jhimmy et al. Smoking-induced aggravation of experimental arthritis is dependent of aryl hydrocarbon receptor activation in Th17 cells. Arthritis Research & Therapy, v. 20, n. 1, 2018Tradução . . Disponível em: https://doi.org/10.1186/s13075-018-1609-9. Acesso em: 03 nov. 2024.
APA
Talbot, J., Peres, R. S., Pinto, L. G., Oliveira, R. D. R., Lima, K. A., Donate, P. B., et al. (2018). Smoking-induced aggravation of experimental arthritis is dependent of aryl hydrocarbon receptor activation in Th17 cells. Arthritis Research & Therapy, 20( 1). doi:10.1186/s13075-018-1609-9
NLM
Talbot J, Peres RS, Pinto LG, Oliveira RDR, Lima KA, Donate PB, Silva JR, Ryffel B, Cunha TM, Alves Filho JCF, Liew FY, Louzada Júnior P, Cunha F de Q. Smoking-induced aggravation of experimental arthritis is dependent of aryl hydrocarbon receptor activation in Th17 cells [Internet]. Arthritis Research & Therapy. 2018 ;20( 1):[citado 2024 nov. 03 ] Available from: https://doi.org/10.1186/s13075-018-1609-9
Vancouver
Talbot J, Peres RS, Pinto LG, Oliveira RDR, Lima KA, Donate PB, Silva JR, Ryffel B, Cunha TM, Alves Filho JCF, Liew FY, Louzada Júnior P, Cunha F de Q. Smoking-induced aggravation of experimental arthritis is dependent of aryl hydrocarbon receptor activation in Th17 cells [Internet]. Arthritis Research & Therapy. 2018 ;20( 1):[citado 2024 nov. 03 ] Available from: https://doi.org/10.1186/s13075-018-1609-9
Artigo de periodico
Pericytes modulate myelination in the central nervous system (2018)
Azevedo, Patrick O.; Sena, Isadora F.G.; Andreotti, Julia P.; Tavares, Juliana Carvalho; Alves Filho, José Carlos Farias; Cunha, Thiago Mattar; Cunha, Fernando de Queiroz; Mintz, Akiva; Birbrair, Alexander
Source: Journal of Cellular Physiology. Unidade: FMRP
Subjects: SISTEMA NERVOSO CENTRAL, ESCLEROSE MÚLTIPLA
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
ABNT
AZEVEDO, Patrick O. et al. Pericytes modulate myelination in the central nervous system. Journal of Cellular Physiology, v. 233, n. 8, p. 5523-5529, 2018Tradução . . Disponível em: https://doi.org/10.1002/jcp.26348. Acesso em: 03 nov. 2024.
APA
Azevedo, P. O., Sena, I. F. G., Andreotti, J. P., Tavares, J. C., Alves Filho, J. C. F., Cunha, T. M., et al. (2018). Pericytes modulate myelination in the central nervous system. Journal of Cellular Physiology, 233( 8), 5523-5529. doi:10.1002/jcp.26348
NLM
Azevedo PO, Sena IFG, Andreotti JP, Tavares JC, Alves Filho JCF, Cunha TM, Cunha F de Q, Mintz A, Birbrair A. Pericytes modulate myelination in the central nervous system [Internet]. Journal of Cellular Physiology. 2018 ; 233( 8): 5523-5529.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1002/jcp.26348
Vancouver
Azevedo PO, Sena IFG, Andreotti JP, Tavares JC, Alves Filho JCF, Cunha TM, Cunha F de Q, Mintz A, Birbrair A. Pericytes modulate myelination in the central nervous system [Internet]. Journal of Cellular Physiology. 2018 ; 233( 8): 5523-5529.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1002/jcp.26348
Artigo de periodico
Modulation of experimental arthritis by vagal sensory and central brain stimulation (2017)
Bassi, Gabriel Shimizu; Dias, Daniel Penteado Martins; Franchin, Marcelo; Talbot, Jhimmy; Reis, Daniel Gustavo; Menezes, Gustavo Batista; Castania, Jaci Airton; Garcia-Cairasco, Norberto; Resstel, Leonardo Barbosa Moraes; Salgado, Hélio César; Cunha, Fernando de Queiroz; Cunha, Thiago Mattar; Ulloa, Luis; Kanashiro, Alexandre
Source: Brain, Behavior, and Immunity. Unidade: FMRP
Subjects: ARTRITE REUMATOIDE, ANTAGONISTAS, SISTEMA NERVOSO SIMPÁTICO, ESTIMULAÇÃO ELÉTRICA, NERVO VAGO
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
ABNT
BASSI, Gabriel Shimizu et al. Modulation of experimental arthritis by vagal sensory and central brain stimulation. Brain, Behavior, and Immunity, v. 64, p. 330-343, 2017Tradução . . Disponível em: https://doi.org/10.1016/j.bbi.2017.04.003. Acesso em: 03 nov. 2024.
APA
Bassi, G. S., Dias, D. P. M., Franchin, M., Talbot, J., Reis, D. G., Menezes, G. B., et al. (2017). Modulation of experimental arthritis by vagal sensory and central brain stimulation. Brain, Behavior, and Immunity, 64, 330-343. doi:10.1016/j.bbi.2017.04.003
NLM
Bassi GS, Dias DPM, Franchin M, Talbot J, Reis DG, Menezes GB, Castania JA, Garcia-Cairasco N, Resstel LBM, Salgado HC, Cunha F de Q, Cunha TM, Ulloa L, Kanashiro A. Modulation of experimental arthritis by vagal sensory and central brain stimulation [Internet]. Brain, Behavior, and Immunity. 2017 ; 64 330-343.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1016/j.bbi.2017.04.003
Vancouver
Bassi GS, Dias DPM, Franchin M, Talbot J, Reis DG, Menezes GB, Castania JA, Garcia-Cairasco N, Resstel LBM, Salgado HC, Cunha F de Q, Cunha TM, Ulloa L, Kanashiro A. Modulation of experimental arthritis by vagal sensory and central brain stimulation [Internet]. Brain, Behavior, and Immunity. 2017 ; 64 330-343.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1016/j.bbi.2017.04.003
Artigo de periodico
Diabetes mellitus and sepsis: A challenging association (2017)
Trevelin, Silvia C.; Carlos, Daniela; Beretta, Matteo; Silva, João Santana da; Cunha, Fernando de Queiroz
Source: Shock. Unidade: FMRP
Subjects: DIABETES MELLITUS, SEPTICEMIA, INSULINA, SEPSE, GLICOSE
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
ABNT
TREVELIN, Silvia C. et al. Diabetes mellitus and sepsis: A challenging association. Shock, v. 43, n. 7, p. 276-287, 2017Tradução . . Disponível em: https://doi.org/10.1097/SHK.0000000000000778. Acesso em: 03 nov. 2024.
APA
Trevelin, S. C., Carlos, D., Beretta, M., Silva, J. S. da, & Cunha, F. de Q. (2017). Diabetes mellitus and sepsis: A challenging association. Shock, 43( 7), 276-287. doi:10.1097/SHK.0000000000000778
NLM
Trevelin SC, Carlos D, Beretta M, Silva JS da, Cunha F de Q. Diabetes mellitus and sepsis: A challenging association [Internet]. Shock. 2017 ; 43( 7): 276-287.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1097/SHK.0000000000000778
Vancouver
Trevelin SC, Carlos D, Beretta M, Silva JS da, Cunha F de Q. Diabetes mellitus and sepsis: A challenging association [Internet]. Shock. 2017 ; 43( 7): 276-287.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1097/SHK.0000000000000778
Artigo de periodico
Chronic toxoplasma gondii infection exacerbates secondary polymicrobial sepsis (2017)
Souza, Maria C.; Fonseca, Denise Morais da ; Kanashiro, Alexandre; Benevides, Luciana; Medina, Tiago S.; Dias, Murilo S.; Andrade, Warrison A.; Bonfá, Giuliano; Silva, Marcondes A. B.; Gozzi, Aline; Borges, Marcos de Carvalho; Gazzinelli, Ricardo T.; Alves Filho, José Carlos Farias; Cunha, Fernando Queiróz; Silva, João Santana da
Source: Frontiers in Cellular and Infection Microbiology. Unidade: FMRP
Subjects: MODELOS ANIMAIS DE DOENÇAS, INTERFERONS, ÓXIDO NÍTRICO, SEPSE, TOXOPLASMOSE
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
ABNT
SOUZA, Maria C. et al. Chronic toxoplasma gondii infection exacerbates secondary polymicrobial sepsis. Frontiers in Cellular and Infection Microbiology, v. 7, 2017Tradução . . Disponível em: https://doi.org/10.3389/fcimb.2017.00116. Acesso em: 03 nov. 2024.
APA
Souza, M. C., Fonseca, D. M. da, Kanashiro, A., Benevides, L., Medina, T. S., Dias, M. S., et al. (2017). Chronic toxoplasma gondii infection exacerbates secondary polymicrobial sepsis. Frontiers in Cellular and Infection Microbiology, 7. doi:10.3389/fcimb.2017.00116
NLM
Souza MC, Fonseca DM da, Kanashiro A, Benevides L, Medina TS, Dias MS, Andrade WA, Bonfá G, Silva MAB, Gozzi A, Borges M de C, Gazzinelli RT, Alves Filho JCF, Cunha FQ, Silva JS da. Chronic toxoplasma gondii infection exacerbates secondary polymicrobial sepsis [Internet]. Frontiers in Cellular and Infection Microbiology. 2017 ;7[citado 2024 nov. 03 ] Available from: https://doi.org/10.3389/fcimb.2017.00116
Vancouver
Souza MC, Fonseca DM da, Kanashiro A, Benevides L, Medina TS, Dias MS, Andrade WA, Bonfá G, Silva MAB, Gozzi A, Borges M de C, Gazzinelli RT, Alves Filho JCF, Cunha FQ, Silva JS da. Chronic toxoplasma gondii infection exacerbates secondary polymicrobial sepsis [Internet]. Frontiers in Cellular and Infection Microbiology. 2017 ;7[citado 2024 nov. 03 ] Available from: https://doi.org/10.3389/fcimb.2017.00116
Artigo de periodico
Toll-like receptor 2 is required for inflammatory process development during leishmania infantum infection (2017)
Sacramento, Laís A.; Costa, Jéssica L. da; Lima, Mikhael H. F. de; Sampaio, Pedro A.; Almeida, Roque P.; Cunha, Fernando Queiróz; Silva, João Santana da; Carregaro, Vanessa
Source: Frontiers in Microbiology. Unidade: FMRP
Subjects: LEISHMANIA INFANTUM, CÉLULAS DENDRÍTICAS, LEISHMANIOSE VISCERAL, NEUTRÓFILOS
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
ABNT
SACRAMENTO, Laís A. et al. Toll-like receptor 2 is required for inflammatory process development during leishmania infantum infection. Frontiers in Microbiology, v. 8, 2017Tradução . . Disponível em: https://doi.org/10.3389/fmicb.2017.00262. Acesso em: 03 nov. 2024.
APA
Sacramento, L. A., Costa, J. L. da, Lima, M. H. F. de, Sampaio, P. A., Almeida, R. P., Cunha, F. Q., et al. (2017). Toll-like receptor 2 is required for inflammatory process development during leishmania infantum infection. Frontiers in Microbiology, 8. doi:10.3389/fmicb.2017.00262
NLM
Sacramento LA, Costa JL da, Lima MHF de, Sampaio PA, Almeida RP, Cunha FQ, Silva JS da, Carregaro V. Toll-like receptor 2 is required for inflammatory process development during leishmania infantum infection [Internet]. Frontiers in Microbiology. 2017 ; 8[citado 2024 nov. 03 ] Available from: https://doi.org/10.3389/fmicb.2017.00262
Vancouver
Sacramento LA, Costa JL da, Lima MHF de, Sampaio PA, Almeida RP, Cunha FQ, Silva JS da, Carregaro V. Toll-like receptor 2 is required for inflammatory process development during leishmania infantum infection [Internet]. Frontiers in Microbiology. 2017 ; 8[citado 2024 nov. 03 ] Available from: https://doi.org/10.3389/fmicb.2017.00262
Artigo de periodico
The Sesquiterpene Lactone, Budlein A, Inhibits Antigen-Induced Arthritis in Mice: Role of NF-κB and Cytokines (2017)
Zarpelon, Ana C.; Fattori, Victor; Pinto, Larissa G.; Pinho-Ribeiro, Felipe A.; Ruiz-Miyazawa, Kenji W.; Turato, Walter Miguel; Cunha, Thiago Mattar; Costa, Fernando Batista da; Cunha, Fernando de Queiróz; Casagrande, Rubia; Arakawa, Nilton S.; Verri Junior, Waldiceu A.
Source: Inflammation. Unidades: FCF, EESC, FCFRP, FMRP
Subjects: ANTÍGENOS, ARTRITE, CITOCINAS, INFLAMAÇÃO, SESQUITERPENOS
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
ABNT
ZARPELON, Ana C. et al. The Sesquiterpene Lactone, Budlein A, Inhibits Antigen-Induced Arthritis in Mice: Role of NF-κB and Cytokines. Inflammation, v. 40, n. 6, p. 2020-2032, 2017Tradução . . Disponível em: https://doi.org/10.1007/s10753-017-0642-1. Acesso em: 03 nov. 2024.
APA
Zarpelon, A. C., Fattori, V., Pinto, L. G., Pinho-Ribeiro, F. A., Ruiz-Miyazawa, K. W., Turato, W. M., et al. (2017). The Sesquiterpene Lactone, Budlein A, Inhibits Antigen-Induced Arthritis in Mice: Role of NF-κB and Cytokines. Inflammation, 40( 6), 2020-2032. doi:10.1007/s10753-017-0642-1
NLM
Zarpelon AC, Fattori V, Pinto LG, Pinho-Ribeiro FA, Ruiz-Miyazawa KW, Turato WM, Cunha TM, Costa FB da, Cunha F de Q, Casagrande R, Arakawa NS, Verri Junior WA. The Sesquiterpene Lactone, Budlein A, Inhibits Antigen-Induced Arthritis in Mice: Role of NF-κB and Cytokines [Internet]. Inflammation. 2017 ; 40( 6): 2020-2032.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1007/s10753-017-0642-1
Vancouver
Zarpelon AC, Fattori V, Pinto LG, Pinho-Ribeiro FA, Ruiz-Miyazawa KW, Turato WM, Cunha TM, Costa FB da, Cunha F de Q, Casagrande R, Arakawa NS, Verri Junior WA. The Sesquiterpene Lactone, Budlein A, Inhibits Antigen-Induced Arthritis in Mice: Role of NF-κB and Cytokines [Internet]. Inflammation. 2017 ; 40( 6): 2020-2032.[citado 2024 nov. 03 ] Available from: https://doi.org/10.1007/s10753-017-0642-1
Artigo de periodico
Lapachol, a compound targeting pyrimidine metabolism, ameliorates experimental autoimmune arthritis (2017)
Peres, Raphael S.; Santos, Gabriela B.; Cecilio, Nerry T.; Jabor, Valquíria Aparecida Polisel; Niehues, Michael; Torres, Bruna G. S.; Buqui, Gabriela; Silva, Carlos Henrique Tomich de Paula da; Costa, Teresa Dalla; Lopes, Norberto Peporine; Nonato, Maria Cristina; Ramalho, Fernando Silva; Louzada Júnior, Paulo; Cunha, Thiago Mattar; Cunha, Fernando de Queiroz; Emery, Flavio da Silva; Alves Filho, José Carlos Farias
Source: Arthritis Research & Therapy. Unidades: FCFRP, FMRP
Subjects: ARTRITE REUMATOIDE, LINFÓCITOS T, FÁRMACOS IMUNOSSUPRESSORES
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
ABNT
PERES, Raphael S. et al. Lapachol, a compound targeting pyrimidine metabolism, ameliorates experimental autoimmune arthritis. Arthritis Research & Therapy, v. 19, n. 1, 2017Tradução . . Disponível em: https://doi.org/10.1186/s13075-017-1236-x. Acesso em: 03 nov. 2024.
APA
Peres, R. S., Santos, G. B., Cecilio, N. T., Jabor, V. A. P., Niehues, M., Torres, B. G. S., et al. (2017). Lapachol, a compound targeting pyrimidine metabolism, ameliorates experimental autoimmune arthritis. Arthritis Research & Therapy, 19( 1). doi:10.1186/s13075-017-1236-x
NLM
Peres RS, Santos GB, Cecilio NT, Jabor VAP, Niehues M, Torres BGS, Buqui G, Silva CHT de P da, Costa TD, Lopes NP, Nonato MC, Ramalho FS, Louzada Júnior P, Cunha TM, Cunha F de Q, Emery F da S, Alves Filho JCF. Lapachol, a compound targeting pyrimidine metabolism, ameliorates experimental autoimmune arthritis [Internet]. Arthritis Research & Therapy. 2017 ; 19( 1):[citado 2024 nov. 03 ] Available from: https://doi.org/10.1186/s13075-017-1236-x
Vancouver
Peres RS, Santos GB, Cecilio NT, Jabor VAP, Niehues M, Torres BGS, Buqui G, Silva CHT de P da, Costa TD, Lopes NP, Nonato MC, Ramalho FS, Louzada Júnior P, Cunha TM, Cunha F de Q, Emery F da S, Alves Filho JCF. Lapachol, a compound targeting pyrimidine metabolism, ameliorates experimental autoimmune arthritis [Internet]. Arthritis Research & Therapy. 2017 ; 19( 1):[citado 2024 nov. 03 ] Available from: https://doi.org/10.1186/s13075-017-1236-x

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