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Since the blockade of endothelin receptors was reported to exert beneficial effects, we investigated the effects of tezosentan, a novel dual endothelin receptor antagonist, in two different experimental models of septic shock induced either by the injection of Escherichia coli endotoxin (ETX, 20 mg/kg, i.p.) or by cecal ligation and puncture (CLP).
However, experimental models of septic shock suggest different results [31],[32].
In animal models of septic shock, fluid resuscitation resulted in modest improvements in a number of physiological variables.
Our results are in contrast to previous findings obtained from different animal models of septic shock [1].
Although the underlying mechanism remains poorly understood, inflammation causing cerebral endothelial activation and blood brain barrier (BBB) alterations were reported in several models of septic brain [1, 2].
In un-resuscitated rodent models of septic shock, the peroxisome proliferator-activated receptor-β/δ (PPAR-β/δ) agonist GW0742 improved visceral organ function.
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The increase of microalbuminuria is a consequence of increased permeability due to inflammatory injury to glomerular endothelium which is frequently observed in clinical practice and experimental models of septic-related acute kidney injury (see above) [ 43].
For example, using a process-modeling approach, a prototype of a DES model of septic shock resuscitation has been developed recently (Figure5) [54].
For example, using a process-modeling approach, a prototype of a DES model of septic shock resuscitation has been developed recently [ 54].
A study was carried out to evaluate the treatment efficiency of modified model of septic tank (ST) for the treatment of domestic wastewater.
Moreover, in a mouse model of septic shock induced by P. aeruginosa LPS, HPA3P2 reduced production of pro-inflammatory mediators and correspondingly reduced lung (alveolar) and liver tissue damage.
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