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Inhibition by soluble mannose (Man) or methyl α-d-mannose (MM) or HM of bacterial adhesion to the bladder cel line in vitro or upon transurethral catheterization into the mouse bladder indicates that the bacteria cannot switch between HM and the mannosylated uroplakins.
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By that time, only the bowel and the urinary bladder indicated any accumulation of radioactivity.
Initial small animal PET data showed high activity concentration in bladder indicating predominantly renal elimination.
Major uptake was found in kidneys and bladder indicating renal excretion.
These results indicate that, at least in the mouse bladder, the instillation of 10 μM PAR4-AP or 100 μM PAR1-AP induces a strong inflammatory reaction characterized by the highest number of PMNs infiltrating the bladder.
For the first time, evidence is presented indicating that VEGF instillation into the mouse bladder promotes a significant increase in peripheral nerve density together with alterations in bladder function and visceral sensitivity.
Fig. 2 Functionalized mesoporous silica nanoparticles (MSN) are taken up by mouse bladder cancer cells.
Care should be taken to express the mouse bladder to avoid additional fluid in the RF field (bladder cannulation should be considered for long-term imaging protocols).
Murine bladder cancer cells (MB49) were found to take up the MSN in vitro; in the mouse bladder, the MSN were taken up preferentially by tumor cells more readily than healthy bladder epithelium.
To understand the basis of bladder-associated pain, we next examined nerve fibers in the mouse bladder.
Treatment with intravesical PAR1, PAR2 and PAR4 agonists induced inflammation in the mouse bladder [21].
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