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Objective:To compare the differences in sleep structure between healthy children and children with cerebral palsy (CP) using polysomnography (PSG).Methods:Fifty-six children aged 1-15 hospitalized for cerebral palsy formed the experimental group, while 30 healthy children served as controls. Both groups were given 24-hour PSG, and their sleep structures were compared and analyzed.Results:The incidence of sleep disorders in the children with cerebral palsy (55.4%) was significantly higher than among the healthy children (20.0%). The average sleep latency was significantly higher than among the healthy children, while the duration and the percentage of the rapid eye movement (REM) stage were significantly lower than among the healthy children. Total sleep time [(458.47±95.62)min], sleep efficiency [(74.26±13.63)%], duration of REM [(68.90±42.70)min] and REM percentage [(13.87±7.12)%] were all significantly lower for the children with severe cerebral palsy than for those with mild or moderate disorder. Their time to wake up after falling asleep was significantly longer. Moreover, the duration of REM and the REM percentage of children with dyskinetic cerebral palsy were significantly lower than for those with spastic cerebral palsy.Conclusions:The incidence of sleep disorders among children with cerebral palsy is higher than among healthy children. They have more difficulty in falling asleep and have a shorter REM stage. Children with severe cerebral palsy and involuntary cerebral palsy have more sleep problems.
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Objective To evaluate the effect of clinical pharmacists on cases consultation by retrospective analysis.Methods Seven hundred and thirty-one consultation cases from January 2011 to December 2014 were systematically reviewed, and the clinical department, question classification, organ system of infection, consultation purpose, recommendation variety to infection problems, acception percentage, infection problem outcome were recorded.Furthermore, the typical cases were analysed.Results The number of consultations and clinical departments increased by years, formulating anti-infective therapeutic regimen, determining duration of therapy and drug dosage were the main purposes of consultation.The proportion of infection problems was 86.0%, adoption rate of recommendations was 83.6%, the clinical efficacy rate was 84.3% among them.The proportion of non-infectious problems was 14.0%, adoption rate of recommendations was 100.0%.Conclusion Clinical pharmacists' professional skills are respected by doctors.Anti-infection problem is a breakthrough point for deeply developing the work of clinical pharmacists.
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Objective To clarify the pathologic change of the motor neuron on spinal cord ischemia reperfusion injury delayed paraplegia. Methods The infrarenal aorta of White New Zealand rabbits (n=24) was occluded for 26 minutes using two bulldog clamps. Rabbits were killed after 8, 24, 72, or 168 hours (n=6 per group), respectively. The clamps was placed but never clamped in sham-operated rabbits (n=24). The lumbar segment of the spinal cord (L5 to L7) was used for morphological studies, including hematoxylin and eosin staining, the expression of bcl-2 and bax proteins in spinal cord was detected with immunohistochemistry. The apoptotic neurons in spinal cord were measured with terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end-labeling of DNA fragments (TUNEL) staining. Results Delayed paraplegia occurred in all rabbits of ischemia reperfusion group at 16-24 hours, but not in sham groups. Motor neurons were selectively lost at 7 days after transient ischemia. After ischemia, the positive expression of bcl-2 protein were in the sham controls but decreased significantly as compared with that of the IR group (P＜0.01), especially in 72 hours reperfusion. The positive expression of bax protein were also in the sham controls, but increased in the IR group, especially in 72 hours reperfusion; In addition, TUNEL study demonstrated that no cells were positively labeled until 24 hours after ischemia, but nuclei of some motor neurons were positively labeled at peak after ischemia reperfusion at 72 hours. Conclusion Spinal cord ischemia in rabbits induces morphological and biochemical changes suggestive of apoptosis. These data raise the possibility that apoptosis contributes to neuronal cell death after spinal cord ischemia reperfusion.
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Objective: To clarify the pathologic change of the motor neuron on spinal cord ischemia reperfusion injury delayed paraplegia. Methods: The infrarenal aorta of White New Zealand rabbits (n=24) was occluded for 26 minutes using two bulldog clamps. Rabbits were killed after 8, 24, 72, or 168 hours (n = 6 per group), respectively. The clamps was placed but never clamped in sham-operated rabbits (n = 24). The lumbar segment of the spinal cord (L5 to L7) was used for morphological studies, including hematoxylin and eosin staining, the expression of bcl-2 and bax proteins in spinal cord was detected with immunohistochemistry. The apoptotic neurons in spinal cord were measured with terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end-labeling of DNA fragments (TUNEL) staining. Results: Delayed paraplegia occurred in all rabbits of ischemia reperfusion group at 16-24 hours, but not in sham groups. Motor neurons were selectively lost at 7 days after transient ischemia. After ischemia, the positive expression of bcl-2 protein were in the sham controls but decreased significantly as compared with that of the IR group (P<0.01), especially in 72 hours reperfusion. The positive expression of bax protein were also in the sham controls, but increased in the IR group, especially in 72 hours reperfusion; In addition, TUNEL study demonstrated that no cells were positively labeled until 24 hours after ischemia, but nuclei of some motor neurons were positively labeled at peak after ischemia reperfusion at 72 hours. Conclusion: Spinal cord ischemia in rabbits induces morphological and biochemical changes suggestive of apoptosis. These data raise the possibility that apoptosis contributes to neuronal cell death after spinal cord ischemia reperfusion.
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BACKGROUND: At present, genetic recombinant technique has been utilized to express recombinant human bone morphogenetic protein-2 (rhBMP-2)and to induce either orthotopic or ectopic regenerated bone successfully. But,because that osteoblastic activity induced by rhBMP-2 is lower than that by natural BMP-2, the perfect vectors have not been discovered yet.OBJECTIVE: BMP recombinant adenovirus (rAdV) was constructed so as to provide feasible vector for the basic treatment of bone defect.DESIGN: Single sample was designed in the experiment.SETTING: Experimental Center of Molecular Biology in First Hospital of Xi'an Jiaotong University.MATERIALS: PACCMV-PLPA plasmid, PJM17 plasmid, 293-cell line.METHODS: The experiment was performed in Experimental Center of Molecular Biology in First Hospital of Xi'an Jiaotong University from September 2001 to June 2002. Reverse Transcription-Polymerase Chain Reaction (RT-PCR) was used to clone the whole-length gene of BMP-2 and construct AdV vector. DNA-calcium phosphate coprecipitation was used to transfect accessory plasmid PJM17 into 293cell and homologous recombination was used to construct rAdV. The titer was assayed and CsC1 density gradient centrifugation and purification were applied.construction of rAdV.binant plasmid is named as pGEM-T/hBMP2, (3 015+1 213)bp in size.It was indicated in agar gel electrophoresis that the practical value was in BMP2 shuttle plasmid: The plasmid was about 10 Kbp in size. Since PACCMV-PLPA plasmid multiclone sites belonged to PUC plasmid series,EcoR Ⅰ enzyme digestion was used to linerarizate recombinant plasmid,10 Kbp in size. 8.8 Kb and 1.2 Kbp visible fragments were obtained durtion of rAdV: PCR technique was used to identify rAdV. The target fragment 1.2Kbp that was amplified by BMP2 specific primer of the whole length was in conformity completely with the theoretic value.CONCLUSION: Successful construction of BMP2 rAdV lays a foundation for the feasible genetic treatment with vector of bone defect.