However, an optimal time window for rehabilitation interventions after hemorrhagic stroke has not been clearly defined. The aim of this study was to determine whether early exercise training initiated 24 h after an intracerebral hemorrhage (ICH) might enhance neurologic recovery more than exercise initiated 1 week after ICH without hematoma expansion and edema volume increase. We subjected adult male Sprague-Dawley rats to experimental ICH by the intrastriatal administration of bacterial collagenase. The rats were randomly divided

into the following 2 groups: early training group (treadmill exercise started 24 h post-ICH: n = 18) and late training group (treadmill exercise started 1-week post-ICH; n = 18). Two weeks after surgery we performed SU5402 manufacturer neurologic tests (rota-rod, modified limb-placing, and adhesive-dot removal tests), and measured hematoma volumes and brain water content. In the late training group, compared with the pre-ICH performance on the rota-rod test (98.3 +/- 69.4 s), the animals had significantly worse performance after the post-ICH rehabilitation (40.5 +/- 52.6 s; p < 0.01, paired t-test). In the early training group however, the motor performance after the post-ICH rehabilitation (56.4 +/- 73.5 s) was not significantly this website different from the baseline pre-ICH performance (79.8 +/- 33.9 s; p = 0.24). There

were no significant differences between the two groups with respect to the other neurologic tests. Early exercise did not increase hematoma size or brain water content. Early treadmill training could be performed safely, and enhanced

motor recovery in a rat model of ICH. Further studies are required to translate the results into clinical significance. (C) 2010 Elsevier Ireland Ltd. All rights reserved.”
“Ribonucleosides inhibit human immunodeficiency virus type 1 (HIV-1) replication by mechanisms that have not been fully elucidated. Here, we report the antiviral mechanism for the ribonucleoside analog 5-azacytidine (5-AZC). We hypothesized that the anti-HIV-1 activity of 5-AZC was due to an increase in the HIV-1 mutation rate following its incorporation into viral RNA during transcription. However, we demonstrate that 5-AZC’s primary antiviral N-acetylglucosamine-1-phosphate transferase activity can be attributed to its effect on the early phase of HIV-1 replication. Furthermore, the antiviral activity was associated with an increase in the frequency of viral mutants, suggesting that 5-AZC’s primary target is reverse transcription. Sequencing analysis showed an enrichment in G-to-C transversion mutations and further supports the idea that reverse transcription is an antiviral target of 5-AZC. These results indicate that 5-AZC is incorporated into viral DNA following reduction to 5-aza-2′-deoxycytidine.