Histamine H2 receptor signaling in the pathogenesis of sepsis: studies in a murine Diabetes model (2013)
- Authors:
- USP affiliated authors: ALVES FILHO, JOSÉ CARLOS FARIAS - FMRP ; SILVA, JOÃO SANTANA DA - FMRP ; CUNHA, FERNANDO DE QUEIROZ - FMRP
- Unidade: FMRP
- DOI: 10.4049/jimmunol.1202907
- Subjects: DIABETES MELLITUS (EXPERIMENTAÇÃO); SEPSE; RECEPTORES (METABOLISMO); BACTEREMIA
- Language: Inglês
- Imprenta:
- Source:
- Título do periódico: Journal of Immunology
- ISSN: 0022-1767
- Volume/Número/Paginação/Ano: v. 191, n. 3, p. 1373-1382, 2013
- Este periódico é de assinatura
- Este artigo é de acesso aberto
- URL de acesso aberto
- Cor do Acesso Aberto: bronze
-
ABNT
CARLOS, Daniela et al. Histamine H2 receptor signaling in the pathogenesis of sepsis: studies in a murine Diabetes model. Journal of Immunology, v. 191, n. 3, p. 1373-1382, 2013Tradução . . Disponível em: https://doi.org/10.4049/jimmunol.1202907. Acesso em: 23 abr. 2024. -
APA
Carlos, D., Spiller, F., Souto, F. O., Trevelin, S. C., Borges, V. F., Freitas, A. de, et al. (2013). Histamine H2 receptor signaling in the pathogenesis of sepsis: studies in a murine Diabetes model. Journal of Immunology, 191( 3), 1373-1382. doi:10.4049/jimmunol.1202907 -
NLM
Carlos D, Spiller F, Souto FO, Trevelin SC, Borges VF, Freitas A de, Alves Filho JCF, Silva JS da, Ryffel B, Cunha F de Q. Histamine H2 receptor signaling in the pathogenesis of sepsis: studies in a murine Diabetes model [Internet]. Journal of Immunology. 2013 ; 191( 3): 1373-1382.[citado 2024 abr. 23 ] Available from: https://doi.org/10.4049/jimmunol.1202907 -
Vancouver
Carlos D, Spiller F, Souto FO, Trevelin SC, Borges VF, Freitas A de, Alves Filho JCF, Silva JS da, Ryffel B, Cunha F de Q. Histamine H2 receptor signaling in the pathogenesis of sepsis: studies in a murine Diabetes model [Internet]. Journal of Immunology. 2013 ; 191( 3): 1373-1382.[citado 2024 abr. 23 ] Available from: https://doi.org/10.4049/jimmunol.1202907 - PI3Kγ/AKT1 signaling in macrophages is essential for resistance against Trypanosoma cruzi infection
- Chronic toxoplasma gondii infection exacerbates secondary polymicrobial sepsis
- Failure of neutrophil migration to infection focus correlates with sepsis outcome: critical role of TLR, nitric-cGMP-PKG pathway and chemokines receptors
- NADPH phagocyte oxidase knockout mice control Trypanosoma cruzi proliferation, but develop circulatory collapse and succumb to infection
- CCR4 controls the suppressive effects of regulatory T cells on early and late events during severe sepsis
- Regulation of type 17 helper T-cell function by nitric oxide during inflammation
- Interleukin-10 rs2227307 and CXCR2 rs1126579 polymorphisms modulate the predisposition to septic shock
- IL-33 signaling is essential to attenuate viral-induced encephalitis development by downregulating iNOS expression in the central nervous system
- PPAR-γ/IL-10 axis inhibits MyD88 expression and ameliorates murine polymicrobial sepsis
- Targeting neutrophils in sepsis
Informações sobre o DOI: 10.4049/jimmunol.1202907 (Fonte: oaDOI API)
How to cite
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
