In addition, we also found that HIF-1 alpha-modified ASCs significantly increased HO-1 expression in cisplatin-induced AKI in vivo. Thus, our study indicated HIF-1 alpha-modified ASCs

implantation could provide advanced benefits in the protection again AKI, which will contribute to developing a new therapeutic strategy for the treatment of AKI.”
“To evaluate the anti-inflammatory activity of topical gel containing nimesulide-loaded nanocapsules using experimental models in vivo, and to compare the anti-inflammatory activity of two nimesulide preparations.\n\nMale Wistar rats (200-250 g) treated with gel containing empty nanocapsules (GEN); gel containing nimesulide in the free form (GNFF) or gel containing nimesulide-loaded nanocapsules (GNN).\n\nNanoprecipitation methods were used to prepare the colloidal suspension. In-vivo experimental models of paw edema, acute BMS-777607 and chronic arthritis, and granuloma formation were used. The gels were applied topically in all models.\n\nThe nanocapsules had an average particle size of 344.6 nm +/- A 4.33 and a polydispersity index of 0.251 +/- A 0.002. The models

of acute inflammation (paw edema and arthritis) showed that GNFF and GNN were able to inhibit the inflammatory process with similar efficacy. Moreover, nanoencapsulation significantly increased the anti-inflammatory activity of nimesulide in two chronic inflammation Bindarit models (chronic arthritis and granuloma). The GNFF- and GNN-induced inhibition of inflammation in the chronic arthritis model were 27.75 and 81.5%, respectively. Similarly, GNFF and GNN reduced granuloma formation by 2.82 and 36.66%.\n\nNanoencapsulation increased the anti-inflammatory activity of topical nimesulide in chronic inflammation models.”
“Dendritic spines of medium spiny neurons represent an essential site of information processing between NMDA this website and dopamine receptors in striatum. Even if activation of NMDA receptors in the striatum has important implications for synaptic plasticity

and disease states, the contribution of specific NMDA receptor subunits still remains to be elucidated. Here, we show that treatment of corticostriatal slices with NR2A antagonist NVP-AAM077 or with NR2A blocking peptide induces a significant increase of spine head width. Sustained treatment with D1 receptor agonist (SKF38393) leads to a significant decrease of NR2A-containing NMDA receptors and to a concomitant increase of spine head width. Interestingly, co-treatment of corticostriatal slices with NR2A antagonist (NVP-AAM077) and D1 receptor agonist augmented the increase of dendritic spine head width as obtained with SKF38393. Conversely, NR2B antagonist (ifenprodil) blocked any morphological effect induced by D1 activation.