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Lingo-1 is a negative regulator of myelination. Repairment of demyelinating diseases, such as multiple sclerosis (MS)/experimental autoimmune encephalomyelitis (EAE), requires activation of the myelination program. In this study, we observed the effect of RNA interference on Lingo-1 expression, and the impact of Lingo-1 suppression on functional recovery and myelination/remyelination in EAE mice. Lentiviral vectors encoding Lingo-1 short hairpin RNA (LV/Lingo-1-shRNA) were constructed to inhibit Lingo-1 expression. LV/Lingo-1-shRNA of different titers were transferred into myelin oligodendrocyte glycoprotein-induced EAE mice by intracerebroventricular (ICV) injection. Meanwhile, lentiviral vectors carrying nonsense gene sequence (LVCON053) were used as negative control. The Lingo-1 expression was detected and locomotor function was evaluated at different time points (on days 1,3,7,14,21, and 30 after ICV injection). Myelination was investigated by luxol fast blue (LFB) staining.LV/Lingo-1-shRNA administration via ICV injection could efficiently down-regulate the Lingo-1 mRNA and protein expression in EAE mice on days 7,14,21, and 30 (P 0.01), especially in the 5 × 10(8) TU/mL and 5 × 10(9) TU/mL LV/Lingo-1-shRNA groups. The locomotor function score in the LV/Lingo-1-shRNA treated groups were significantly lower than the untreated or LVCON053 group from day 7 on. The 5 × 10(8) TU/mL LV/Lingo-1-shRNA group achieved the best functional improvement (0.87 ± 0.11 vs. 3.05 ± 0.13, P 0.001). Enhanced myelination/remyelination was observed in the 5 × 10(7) , 5 × 10(8) , 5 × 10(9) TU/mL LV/Lingo-1-shRNA groups by LFB staining (P 0.05, P 0.01, and P 0.05).The data showed that administering LV/Lingo-1-shRNA by ICV injection could efficiently knockdown Lingo-1 expression in vivo, improve functional recovery and enhance myelination/remyelination. Antagonism of Lingo-1 by RNA interference is, therefore, a promising approach for the treatment of demyelinating diseases, such as MS/EAE.

To explore the efficacy and safety of ropinirole in the treatment of Parkinson's disease.From November 2005 to April 2007, a total of 221 subjects from 7 hospitals of Beijing, Lanzhou and Wuhan participated in a 12-week multi-center, randomized, bromocriptine-controlled, double-blind, double-dummy and parallel-group trial. The efficacy of ropinirole was assessed with the unified Parkinson's disease rating scale (UPDRS) score, "off" time according to the patient's diary and the overall evolution of clinical efficacy. The safety was assessed on the basis of adverse events, blood pressure, pulse, laboratory measurement and electrocardiographic recordings. And the statistical analyses were performed with t, paired t, χ(2) and covariance tests.In the intent-to-treat population, the average UPDRSIII score decreased to (11 ± 9) in ropinirole group and (11 ± 10) in bromocriptine group while the UPDRSIIscore decreased to (4 ± 4) and (3 ± 5) respectively at Week 12 versus baseline. It showed that ropinirole was non-inferior to bromocriptine. The "off" time at Week 12 [(3.0 ± 1.2)h, (3.8 ± 1.6)h] versus baseline [(4.2 ± 2.0)h, (4.4 ± 1.7)h] decreased (t = 10.772, t = 5.746, P = 0.000) in ropinirole and bromocriptine groups. Ropinirole offered a better overall improvement rate (q = 7.241, P = 0.007). The adverse events occurring at a ratio of over 5% caused by ropinirole included orthostatic hypotension, nausea, dizziness, upper abdominal discomfort, insomnia and palpitation. No significant difference existed in the frequency of adverse events between two groups.Ropinirole is both effective and safe in the treatment of Chinese patients with Parkinson's disease.

To compare the efficacy of midazolam and diazepam for treatment of acute seizures in children.One hundred and twenty children with acute seizures were randomly divided into two groups: midazolam (0.1-0.3 mg/kg) and diazepam treatment (0.3-0.5 mg/kg) (n=60 each). In cases with seizure recurrence or statural convulsivus, a maintenance dose of midazolam (1-8 mg/kg per hour) and a maintenance dose of diazepam (0.5-1 mg/kg per hour) or along with phenobarbital sodium were given in the midazolam and diazepam treatment groups, respectively. The therapeutic effects were compared between the two groups.The seizures were relieved in all cases from the two groups 10 minutes after administration of midazolam or diazepam. There were no significant differences in the average time of seizure control between the two groups. Five children in the midazolam group had seizure recurrence or statural convulsivus after 10 minutes compared with 13 children in the diazepan group (P0.05). The time of seizure control averaged 40+/-32 minutes in the midazolam group compared with 69+/-24 minutes in the diazepam group after maintenance treatment (P0.05). No midazolam and diazepam treatment related adverse events were observed.Midazolam is safe and effective in the treatment of acute seizures in children. Midazolam appears to be a better option in the treatment of recurrent seizures or statural convulsivus than diazepam.

To investigate the mechanism of myocardial ischemia/reperfusion injury and the protective effect of fructose-1, 6-diphosphagic (FDP) and dexamethasone (DXM) in hemorrhagic shock in rabbits.Using a hemorrhagic shock model of Wiggers, 48 rabbits were randomly divided into 6 groups. Group I control group; GroupII with drugs given before ischemia phase (divided into 3 groups: FDP I, DXM I and FDP I+ DXM I); Group III with drugs given in reperfusion phase (divided into 2 groups: FDPII and DXMII). The levels of creatine kinase (CK) and troponin I (cTnI) in plasma were measured, and myocyte apoptosis index was assessed.Baseline levels of CK and cTnI were similar in three groups; CK and cTnI and apoptosis index were lower or with a lower tendency in groupII and in groupIII (P0.05 or P0.01); CK and cTnI showed a lower tendency in rise in FDP I and DXM I than in FDPII and even slower in FDP group than in DXM group; CK and cTnI levels rose slower in FDP I+DXM I than in FDP I and DXM I.FDP given during ischemia and DXM could effectively protect the myocardium from reperfusion injury following hemorrhagic shock.