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Objective To systematically explore the efficacy of four intervention regiments including desmopressin, alarm, desmopressin combined with alarm, and desmopressin combined with anticholinergic drugs in the treatment of monosymptomatic nocturnal enuresis in children by network meta-analysis. Methods The databases of PubMed, Cochrance Library, EMBase and Web of Science were systematically searched and retrieved upto August 1, 2017. Included were the randomized controlled trials (RCTs) which had any two or more of four intervention regiments (desmopressin, alarm, desmopressin combined with alarm, and desmopressin combined with anticholinergic drugs) for treatment of monosymptomatic nocturnal enuresis in children. The literature was screened according to the established inclusion and exclusion criteria, and the data extraction and quality evaluation were performed for the final inclusion of RCT. Software R 3.3.2 and STATA 14.0 were used for data analysis. Results Fifteen RCTs were included with a total of 1505 children. Network meta-analysis showed that the complete response rate and success rate of desmopressin combined with anticholinergic drugs were higher than those of desmopressin (complete reaction rate: OR=2.8, 95％ CI :1.5～5.4; success rate: OR=3.5, 95％ CI :1.7～7.5) and alarm (complete response rate: OR=2.7, 95％ CI :1.1～6.6; success rate: OR=3.8, 95％ CI: 1.6～9.0. The success rate of desmopressin combined with alarm was higher than that of alarm (OR=1.9, 95％CI: 1.1～3.4) . The recurrence rate of alarm after treatment was significantly lower than that of desmopressin (OR=0.15, 95％CI: 0.03～0.53) . The ranking results showed that the complete response rate and success rate of desmopressin combined with anticholinergic drugs were the best. The desmopressin combined with alarm can minimize the number of bed-wetting episodes per week and the recurrence rate of alarm was the lowest among the four regiments. Conclusion The effect of desmopressin combined with anticholinergic drugs is significantly better than that of alarm or desmopressin alone. The combination of desmopressin and alarm has a slight advantage or similar effect to that of single alarm or desmopressin treatment. The effect of desmopressin is similar to that of alarm. Alarm treatment has the lowest recurrence rate.
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Objective To evaluate the effects of ganglioside GM1 on hypoxic ischemic brain damage (HIBD) in neonatal rats and on the expression of potassium-chloride cotransporter 2 (KCC2) in hippocampus.Methods Seven-day-old Sprague-Dawley (SD) rats (n=72) were randomly divided into a sham group,an HIBD group and a ganglioside GM1 group.Each group was further divided into a 3 d subgroup and a 21 d subgroup according to the different detection index (n=12).Rat HIBD models were prepared according the Rice-Vannucci method.After HIBD,the ganglioside GM1 group was given ganglioside GM1 20 mg/ (kg ·d) by intraperitoneal injection for 3 d continuously.2-,3-,5-triphenyltetrazolium chloride (TTC) was preformed to evaluate the area of cerebral infarction of HIBD in each 3 d subgroup.Spontaneous activity recorder was used to observe the locomotor activity of the rats in the 21 d subgroups.Morris water maze test was conducted for assessment of rats' learning and memory abilities in the 21 d subgroups.Western blot analysis was employed to determine the alterations in KCC2 expression in hippocampus in all the 3 d and 21 d subgroups.Results Compared with the HIBD group (28.6％±5.2％),the ratio of cerebral infarction volume in the ganglioside GM1 group (11.3％±2.4％) was significantly reduced (P＜0.05).Compared with the HIBD group (289.6±61.3),the number of locomotor activities within 2 h in the ganglioside GM1 group (412.1±66.8) was significantly increased (P＜0.05).Compared with the HIBD group,the escape latency was significantly reduced,but the percentage time of target quadrant and the number of crossing the platform were significantly increased in the ganglioside GM1 group (P＜0.05).Three days and 21 days after HIBD,the expression of KCC2 in the ganglioside GM1 group was significantly higher than that in the HIBD group (P＜0.05).Conclusion Ganglioside GM1 may have a significant protective effect on HIBD in neonatal rats,and its mechanism may be related to regulation of the expression of KCC2 in hippocampus.
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Objective To study the occurrence of acute gastrointestinal injury under different critical status in Pediatric Intensive Care Unit,and to assess the connection between citrulline and acute gastrointestinal injury.To ana-lyze the correlation among serum citrulline and C-reaction protein(CRP),procalcitonin(PCT),creatinine,urea nitro-gen,bilirubin,lactate,albumin.To study the role of citrulline in evaluating the children condition,prognosis and changes in critically ill children.Methods Ninety-six pediatric patients who were critically ill at the Pediatric Intensive Care Unit of the Second Hospital of Lanzhou University were selected,excluding those with primary gastrointestinal diseases and chronic kidney disease.Clinical features were recorded and CRP,PCT,creatinine,urea nitrogen,bilirubin,lactate, and albumin were measured.Serum citrulline concentrations were measured by high performance liquid chromatography in 65 patients with gastrointestinal injury,and sensitivity,specificity and area under the receiver operating characteristic (ROC)curve were calculated.Results The incidence of acute gastrointestinal injuries in non-critical group,critical group,reorganization critical group were 47.06%(16/34 cases),75.00%(36/48 cases),92.86%(13/14 cases) (χ2=11.848,P=0.003).The serum citrulline concentrations of gastrointestinal injury group and non- gastrointesti-nal injury group were(14.655 ± 8.231)μmol/L,(23.522 ± 11.079)μmol/L(t=4.398,P<0.05).The area under ROC of citrulline was 0.079 8.Serum citrulline concentrations increased significantly in infants with very severe gastro-intestinal injury after 3 days of treatment compared with admission[(26. 40 ± 16. 10)μmol/L vs.(14. 40 ± 6.82)μmol/L,t=5.524,P=0.029].The lower serum citrulline levels the children had,the higher mortality was. There were negative correlations among serum citrullin and CRP,PCT and length of hospital stay(r = -0. 319,-0.299,-0.364,P=0.003,0.006,0.001).There were no correlations among serum citrullin and blood urea nitro-gen,lactic acid,albumin,and bilirubin levels.Conclusion The more critically ill children have a higher incidence of acute gastrointestinal injury and the worse the prognosis.Serum citrulline levels may well reflect the extent of acute gas-trointestinal injury and the outcome.Perhaps it can be one of the reliable markers to evaluate the function of gastrointes-tinal and participate in assessing critical condition and prognosis in critical ill children ness.
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<p><b>OBJECTIVE</b>To investigate the therapeutic effect of thyroid hormone in nude mice bearing human pancreatic cancer xenograft.</p><p><b>METHODS</b>A BALB/c nude mouse model bearing pancreatic cancer was established with human pancreatic cancer cell line Bx-PC3. The mouse models were divided randomly into 5 groups, namely the control group treated with distilled water, high and low concentrations of thyroid hormone (T3) groups, and high and low concentration of propylthiouracil (PTU) groups. After intervention for 21 days, the changes in body weight and xenograft tumor volume and weight were measured, and the serum T3 concentration was detected by ELISA assay. The expression of proliferating cell nuclear antigen (PCNA) and microvessel density (MVD) were detected using immunohistochemistry.</p><p><b>RESULTS</b>The body weight of nude mice in T3 groups was significantly reduced after intervention, while that in PTU groups showed no obvious changes. Compared with PTU groups and control group, T3 groups showed significantly reduced tumor volume and weight (P<0.05) with also reduced PCNA expression and MVD, but these effect did not exhibit a dose dependence (P>0.05).</p><p><b>CONCLUSION</b>Thyroid hormone can inhibit the growth of human pancreatic cancer in nude mice by suppressing the proliferation and angiogenesis of the tumor cells, suggesting the potential value of thyroid hormone in pancreatic cancer therapy.</p>