|1.||Baliga, Reshma S: 1 article (08/2014)|
|2.||Hobbs, Adrian J: 1 article (08/2014)|
|3.||MacAllister, Raymond J: 1 article (08/2014)|
|4.||Bubb, Kristen J: 1 article (08/2014)|
|5.||Patel, Jigisha: 1 article (08/2014)|
|6.||Trinder, Sarah L: 1 article (08/2014)|
|7.||Clapp, Lucie H: 1 article (08/2014)|
|8.||Lu, Ruirui: 1 article (08/2014)|
|9.||Geisslinger, Gerd: 1 article (08/2014)|
|10.||Real, Catherine I: 1 article (08/2014)|
08/05/2014 - "BAY 60-7550 prevented the onset of both hypoxia- and bleomycin-induced PH and produced a significantly greater reduction in disease severity when given in combination with a neutral endopeptidase inhibitor (enhances endogenous natriuretic peptides), trepostinil, inorganic nitrate (NO donor), or a PDE5 inhibitor. "
08/01/2014 - "Administration of the selective PDE2A inhibitor, BAY 60-7550, increased the nociceptive behavior of mice in animal models of inflammatory pain. "
08/01/2014 - "Moreover, BAY 60-7550 increased the pain hypersensitivity induced by intrathecal delivery of cyclic adenosine monophosphate, but not of cyclic guanosine monophosphate, and it increased the cyclic adenosine monophosphate levels in spinal cord tissues. "
08/01/2014 - "Effects of the selective PDE2A inhibitor, BAY 60-7550 (Cayman Chemical, Ann Arbor, MI), in animal models of inflammatory pain (n = 6 to 10), neuropathic pain (n = 5 to 6), and after intrathecal injection of cyclic nucleotides (n = 6 to 8) were examined. "
|3.||Neuralgia (Stump Neuralgia)
|4.||Memory Disorders (Memory Loss)
01/01/2013 - "We concluded that since BAY 60-7550 and PQ10 reversed both scopolamine- and MK-801-induced memory deficits, this supports the notion that dual substrate PDE inhibitors might be suitable candidates for cognition enhancement."
01/01/2013 - "Both BAY 60-7550 (1mg/kg) and PQ-10 (0.3mg/kg) attenuated the scopolamine-induced memory deficit. "
|2.||Neprilysin (Neutral Endopeptidase)
|6.||5'-Guanylic Acid (GMP)
|7.||Adenosine Monophosphate (AMP)
|8.||tranilast (N 5')