A live bacteria SERS platform for the in situ monitoring of nitric oxide release from a single MRSA

2018 ◽  
Vol 54 (51) ◽  
pp. 7022-7025 ◽  
Author(s):  
Zhijun Zhang ◽  
Xuemei Han ◽  
Zhimin Wang ◽  
Zhe Yang ◽  
Wenmin Zhang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
In Situ Monitoring ◽  
Nitric Oxide Release ◽  
Live Bacteria

A live bacteria SERS platform is developed for the precise and sensitive monitoring of nitric oxide release from a single MRSA.

Improving tumor hypoxia and radiotherapy resistance via in situ nitric oxide release strategy

2020 ◽  
Vol 150 ◽  
pp. 96-107
Author(s):  
Jingyao Tu ◽  
Kun Tu ◽  
Haoran Xu ◽  
Lei Wang ◽  
Xianglin Yuan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Tumor Hypoxia ◽  
Nitric Oxide Release ◽  
Radiotherapy Resistance ◽  
Release Strategy

Nitric oxide release from a single cell measured in situ by a porphyrinic-based microsensor

Nature ◽  
1992 ◽  
Vol 358 (6388) ◽  
pp. 676-678 ◽  
Author(s):  
Tadeusz Malinski ◽  
Ziad Taha
Keyword(s):  
Nitric Oxide ◽  
Single Cell ◽  
Nitric Oxide Release

Simultaneous in situ monitoring of intracellular Ca2+ and NO in endothelium of coronary arteries

2002 ◽  
Vol 283 (6) ◽  
pp. H2725-H2732 ◽  
Author(s):  
Fu-Xian Yi ◽  
Andrew Y. Zhang ◽  
William B. Campbell ◽  
Ai-Ping Zou ◽  
Cornelis van Breemen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Coronary Arteries ◽  
High Speed ◽  
Tyrosine Phosphatase ◽  
In Situ Monitoring ◽  
No Production ◽  
Slow Increase ◽  
Intracellular Ca ◽  
Endothelial Nitric Oxide

We developed an in situ assay system to simultaneously monitor intracellular Ca2+concentration ([Ca2+]i, fura 2 as indicator) and nitric oxide (NO) levels [4,5-diaminofluorescein as probe] in the intact endothelium of small bovine coronary arteries by using a fluorescent microscopic imaging technique with high-speed wavelength switching. Bradykinin (BK; 1 μM) stimulated a rapid increase in [Ca2+]i followed by an increase in NO production in the endothelial cells. The protein tyrosine phosphatase inhibitor phenylarsine oxide (PAO; 10 μM) induced a gradual, small increase in [Ca2+]i and a slow increase in intracellular NO levels. Removal of extracellular Ca2+ and depletion of Ca2+ stores completely blocked BK-induced increase in NO production but had no effect on PAO-induced NO production. However, a further reduction of [Ca2+]i by application of BAPTA-AM or EGTA with ionomycin abolished the PAO-induced NO increase. These results indicate that a simultaneous monitoring of [Ca2+]i and intracellular NO production in the intact endothelium is a powerful tool to study Ca2+-dependent regulation of endothelial nitric oxide synthase, which provides the first direct evidence for a permissive role of Ca2+ in tyrosine phosphorylation-induced NO production.

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