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High doses of dexamethasone (Dex) or myostatin (Mstn) induce severe atrophy of skeletal muscle. Here we show a novel microRNA1 (miR1)-mediated mechanism through which Dex promotes skeletal muscle atrophy. Using both C2C12 myotubes and mouse models of Dex-induced atrophy we show that Dex induces miR1 expression through glucocorticoid receptor (GR). We further show that Mstn treatment facilitates GR nuclear translocation and thereby induces miR1 expression. Inhibition of miR1 in C2C12 myotubes attenuated the Dex-induced increase in atrophy-related proteins confirming a role for miR1 in atrophy. Analysis of miR1 targets revealed that HSP70 is regulated by miR1 during atrophy. Our results demonstrate that increased miR1 during atrophy reduced HSP70 levels, which resulted in decreased phosphorylation of AKT, as HSP70 binds to and protects phosphorylation of AKT. We further show that loss of pAKT leads to decreased phosphorylation, and thus, enhanced activation of FOXO3, up-regulation of MuRF1 and Atrogin-1, and progression of skeletal muscle atrophy. Based on these results, we propose a model whereby Dex- and Mstn-mediated atrophic signals are integrated through miR1, which then either directly or indirectly, inhibits the proteins involved in providing protection against atrophy.

Objective: To study the underlying mechanism of electroacupuncture (EA) in relieving epilepsy in pentylenetetrazole (PTZ)-induced epilepsy rats., Methods: Twenty SD rats were randomly divided into normal control, model, EA, Nimodipine groups, with 5 cases in each. Epilepsy model was established by intraperitoneal injection of PTZ (32.0 mg/kg), once daily for 28 days. EA (100 Hz, 0.6 mA) was applied to "Baihui" (GV 20) and "Dazhui" (GV 14), once daily for 7 days. For Nimodipine group, the rats were given with nimodipine (0.25 mg/kg, i.p.), once daily for 7 days. Electroencephalogram (EEG) was recorded and the fluorescence intensity of Ca2+ of the hippocampus tissue sections was detected by laser scanning confocal microscope (LSCM) after incubation in artificial cerebrospinal fluid containing Flou-3/AM (10 micromol/L) and pluronic F-127 (5 microl)., Results: Compared with model group, the latencies of epileptic EEG seizure prolonged obviously (P < 0.05), and epileptic EEG seizure frequencies decreased significantly (P < 0.05) in EA and Nimodipine groups. The fluorescence intensity of intracellular Ca2+ in hippocampus tissue in model group was obviously higher than that in control group (P < 0.01). In comparison to model group, Ca2+ levels in EA and Nimodipine groups lowered considerably (P < 0.05, P < 0.01). No significant differences were found between EA and Nimodipine groups in the aforementioned 3 indexes (P > 0.05)., Conclusion: EA has an obvious anti-epileptic effect, which may be closely related to its effect in downregulating the increased hippocampal Ca2+ level in PTZ-kindled epilepsy rats.

Objective: To investigate the physiologic course of third stage of labor, and to judge the optimal time of natural placental separation permitted., Methods: To observe and record the course of third stage of labor by continuous dynamic ultrasonography and to estimate the total amount of blood loss from placental separation within two hours after delivery by the method of weighing lost blood., Results: Third stage of labor can be divided into four phases: the latent phase (4.37 +/- 3.78) min, the contraction phase (1.48 +/- 0.97) min, the detachment phase (0.50 +/- 0.00) min, and the expulsion phase (0.62 +/- 2.23) min. In 85% of the puerperas the third stage of labor takes about 10 minutes (average 6.94 minutes). The amount of postpartum hemorrhage and the risk of the patient increased prominently if the time of stage of labor was longer than 10 minutes (P < 0.01)., Conclusion: The third stage of labor must be limited in 10 minutes to prevent postpartum hemorrhage.