scholarly journals Perturbations in nitric oxide homeostasis promote Arabidopsis disease susceptibility towards Phytophthora parasitica

2021 ◽  
Author(s):  
Beimi Cui ◽  
Xiangren Ma ◽  
Yuan Li ◽  
Yu Zhou ◽  
Xiuyun Ju ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Disease Susceptibility ◽  
Phytophthora Parasitica

Influence of the inducible nitric oxide synthase gene (NOS2A) on inflammatory bowel disease susceptibility

2007 ◽  
Vol 59 (11) ◽  
pp. 833-837 ◽  
Author(s):  
M. Carmen Martín ◽  
Alfonso Martinez ◽  
J. Luis Mendoza ◽  
Carlos Taxonera ◽  
Manuel Díaz-Rubio ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Bowel Disease ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Bowel Disease ◽  
Disease Susceptibility ◽  
Inflammatory Bowel ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Genetic susceptibility to leishmanial infections: studies in mice and man

Parasitology ◽  
1996 ◽  
Vol 112 (S1) ◽  
pp. S67-S74 ◽  
Author(s):  
J. M. Blackwell
Keyword(s):  
Nitric Oxide ◽  
Mouse Chromosome ◽  
Macrophage Activation ◽  
Disease Susceptibility ◽  
Susceptibility Genes ◽  
T Cell Subsets ◽  
Chromosome 17 ◽  
T Helper ◽  
Chromosome 11 ◽  
T Helper 2

SUMMARYTwo important recent advances inLeishmaniaimmunology are: (i) the demonstration of a dramatic dichotomy in T helper 1 versus T helper 2 subset expansion leading to protection versus disease exacerbation; and (ii) analysis of the macrophage activation pathways leading to enhanced intracellular killing of parasites, in particular the tumour necrosis factor α (TNFα)-dependent sustained induction of the inducible nitric oxide synthase gene (Nos2) leading to the generation of large amounts of nitric oxide (NO). Given the broad spectrum of disease phenotypes in human leishmaniasis, one might predict that a genetic defect at any key point in this macrophage activation pathway and/or in pathways leading to activation of different T cell subsets, and the latter may be a pleiotropic effect of the former, will contribute to disease susceptibility. By studying disease in genetically-defined inbred mouse strains, it has been possible to identify 5 regions of the murine genome carrying leishmanial susceptibility genes. The genes include: (i)Scl-2(mouse chromosme 4/human chromosome 9p; candidate Janus tyrosine kinase 1) controlling a unique no lesion growth resistance phenotype toLeishmania mexicana; (ii)Scl-1(distal mouse chromosome 11/human 17q; candidatesNos2, Sigje, MIP1α, MIP1β) controlling healing versus non-healing responses toL. major; (iii) the ‘T helper 2’ cytokine gene cluster (proximal murine chromosome 11/human 5p; candidates IL4,5,9) controlling later phases ofL. majorinfection; (iv) the major histocompatibility complex (MHC: H-2 in mouse, HLA in man: mouse chromosome 17/human 6p; candidates class II and class III including TNFα/β genes); and (v)Nramp1, the positionally cloned candidate for the murine macrophage resistance geneIty/Lsh/Bcg(mouse chromosome 1/human 2q35). This review examines these 5 regions and the candidate genes within them, reflecting on their current status as candidates for human disease susceptibility genes.

Localization of endothelial nitric oxide synthase in the normal and failing human atrial myocardium

1996 ◽  
Vol 54 ◽  
pp. 786-787
Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Cardiac Tissues ◽  
Mammalian Tissues ◽  
End Stage Heart Failure ◽  
End Stage ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).

Nitric Oxide Reduces Pressor Responsiveness During Ovine Hypoadrenocorticism

2001 ◽  
Vol 28 (5-6) ◽  
pp. 459-462
Author(s):  
Pini Orbach ◽  
Charles E Wood ◽  
Maureen Keller-Wood
Keyword(s):  
Nitric Oxide

Nitric oxide synthase and cellac disease

2001 ◽  
Vol 120 (5) ◽  
pp. A684-A684
Author(s):  
I DANIELS ◽  
I MURRAY ◽  
W GODDARD ◽  
R LONG
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Oxide Synthase
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