Objective To observe the effect of evidence-based nursing on improvement of preoperative fears and perioperative quality of life in patients undergoing general surgery. Methods 160 cases of general surgery patients in our hospital from September 2009 to September 2010 were chosen as the research object.The 160 cases were divided into the control group and the observation group with 80 cases in each group.The control group was taken with perioperative routine care.The observation group was given evidence-based nursing.The preoperative fear score (FAVS),perioperative quality of life (QOL)score and treatment compliance for the two groups were compared. Results The fear scores for the two groups of patients before treatment were compared.The score in the observation group was significantly lower than the control group,the difference was significant.The scores of preoperative and postnperative quality of life for the two groups were compared.The patients of the observation group were significantly higher than the patients of the control group,the difference between the two groups was significant.The treatment compliance of the observation group was better than that of the control group. Conclusions The evidence- based nursing model can improve preoperative fears and perioperative quality of Wife of patients undergoing general surgery,improve patients' treatment compliance,and promote the success of operation and recovery of patients.It is worthy of clinical application.

Objective To investigate the role of electromyography(EMG) in diagnosis of nervous system diseases in children.(Met)-hods EMG tests were carried out in 354 patients with nervous system diseases,and the data and results of EMG tests were analyzed.Results One hundred and sixty-six patients′ results of EMG were abnormal.Among these abnormalities,36 cases were myogenic,47 cases were neurogenic,abnormalities of 69 cases were located in peripheral nerves,3 cases got positive in repetitive nerve stimulation(RNS),and 11 cases were on the borderline.In 36 myogenic patients,clinical diagnosis were as follow: progressive muscular dystrophy(PMD,18 cases),polymyositis(2 cases),mitochondrial encephalomyopathy(1 case), and the other 15 cases had no definite diagnosis.In 47 neurogenic patients,the diagnosis were spinal muscular atrophy(SMA,29 cases),sequela of poliomyelitis(2 cases),acute transverse myelitis(ATM,4 cases),and the other 12 patients had no definite diagnosis.In 69 cases of peripheral nerve abnormality,diagnosis were injury of brachial nerve(23 cases),hereditary motor sensory neuropathy(HMSN,2 cases),Guillain-Barre syndrome(GBS,9(ca)-ses),chronic inflammatory demyelinating polyradiculoneuropathy(CIDP,1 case),injury of facial nerve(4 cases),injury of common(pe)-roneal nerve(6 cases),metachromatic leukodystrophy(MLD,1 case),and the other 23 patients had no definite diagnosis.Three patients who got RNS positive were all diagnosed myasthenia gravis(MG),and ocular type(1 case),general type(2 cases).Eleven patients whose EMG results were borderline were all diagnosed indefinitely.One hundred and eighty-eight patients had normal results of EMG test.The diagnosis of these patients were included ocular MG(21 cases),cerebral palsy(CP,5 cases),ATM(2 cases),polymyositis((1 case)),and some other nervous system diseases(21 cases),and the other 138 were diagnosed indefinitely.Conclusions 1.EMG plays an important role in definite diagnosis of PMD,SMA,poliomyelitis and nerve injury;2.EMG can provide clue or basis in the differential(dia)gnosis of nervous system diseases which involved lower motor unit;3.EMG test has very low positive results in children with MG;(4.EMG) has little help in diagnosis of diseases involved upper motor unit only.

Objective To observe the expression of mitochondrial fission protein locus Fis1 and ultrastructural changes in the renal cells of rats with chronic fluorosis,and to reveal the mechanism in mitochondrial damage of the renal cells.Methods Sixty SD rats were randomly divided into 3 groups according to sex and body mass(20 in each group):control group,lower fluoride group and higher fluoride group.All the rats were fed with different doses of sodium fluoride in drinking water(0,10 and 50 mg/L,respectively).Six-month later,the expression of Fisl in renal cells was determined by real-time fluorenscence quantitative PCR and immunohistochemistry technology,the mitochondrial morphology of renal cells was observed under transmission electron microscopy (TEM).Results As compared with the control group(28.70 ± 12.41),Fis1 mRNA levels(91.48 + 34.83 and 582.09 ± 184.69) in renal cells of the lower fluoride and the higher fluoride groups were increased(all P ＜ 0.05).As compared with the control group(10.49 ± 7.66),Fisl protein levels(16.33 ± 10.26 and 21.50 ± 5.24) in renal cells of the lower fluoride and the higher fluoride groups showed a trend of increasing,the higher fluoride group was higher than that of the control group(P ＜ 0.05).By TEM,mitochondrial crest in renal cells of the lower fluoride and the higher fluoride groups was vague or disappeared,mitochondrial division section appeared.Conclusions Fluoride is a kind of toxicant that can cause damage to mitochondrion of renal cells,induce the expression of Fis1 in transcriptional and protein level,and lead to the obstacles of mitochondrial fusion-fission and ultrastructural abnormality of mitochondrion,which may play an important role in mechanism of mitochondrial damage in the renal cells of rats with chronic fluorosis.

Objective To explore the lethal action and possible mechanism of RI-1, a RAD51 inhibitor, on MSH2 deficient colorectal cancer cells.Methods The expression of MSH2 protein level was assessed by Western blot, and the sensibility of human colorectal cancer cells to RI-1 (10, 20, 30, 40 and 50 μmol/L)was measured by MTT method.Lentivirus vectors MSH2-shRNA and Neg-shRNA (negative control) were constructed and transfected into HT29 cell.Apoptosis and DNA damage of cells treated with RI-1(40 μmol/L)were detected by flow cytometry and Single cell gel electrophoresis respectively.In addition, the formation of γ-H2AX foci was analyzed by immunofluorescence.Results Compared with control, MSH2-deficient HCT8 cells had obviously apoptosis(P<0.01);in HCT8 and HT29 Shmsh2 cells, tail DNA%, tail length, tail moment and olive tail moment were markedly increased(P<0.05),and the number of γ-H2AX focus were increased(P<0.01).Conclusions RAD51 inhibitor RI-1 selectively kills MSH2 deficient colorectal cancer cells by increasing DNA damage.

Objective To investigate the clinical and electroencephalogram (EEG) characteristics of children with electrical status cpilepticus during sleep (ESES), and the response to medication therapy. Methods AEEG and VEEG including an entire sleeping c-ycle were performed on 26 patients with ESES. The clinical and EEG changes, neuropsychological impairment and the response to medication therapy were followed up. Results Twenty five patients had seizures,21 cases had normal psychomotor development before ESES. After the onset of the disease,Fifteen cases developed language disorder, 16 cases developed psychological and behavior abnormalities, 13 cases had both of the problems Seventeen patients belonged to epileptic syndrome. Patients in this cohort had good response to clonazepam and valproate treatment. Cortical steroid could dispel the electrical discharge. Eighteen patients had been followed up. Seizures stopped in 15 cases after treatment ESES disappeared in 16 cases, 4 of them still had neuropsychological impairment ESES sustained in 2 cases Conclusions ESES is a specific EEG phenomenon. Continue epileptic form discharge during non - rapid cye movement sleep is the major cause of neuropsychological impairment in patients with ESES. To control the seizures and electrical state are very important for the prevention and treatment of neuropsychological impairment.

Objective The aim of the study was to investigate the expression of P-glycoprotein (P-gp)and nuclear factor κB (NF-κB) in the cerebral cortex of rat with chronic fluorosis,and to reveal the mechanisms of damaged nervous system resulted from the toxicity of fluoride.Methods Sixty SD rats were randomly divided into three groups.The rats in each group were given drinking water containing different levels of fluoride:control group less than 0.5 mg/L,small amount of fluoride exposure group 10.0 mg/L and large amount of fluoride exposure group 50.0 mg/L.The animals were examined at the sixth month after initiating the experiment.Protein levels of P-gp and NF-κB in brain tissues were detected by immunocytochemistry and Western blotting,and the P-gp protein and mRNA level by quantitative real time PCR method.Results As compared to the control group(28.21 ±6.13),the numbers of positive staining cells by P-gp antibody in the cortex of rat brains were significantly increased in both the small and the large amount of fluoride exposure groups[(48.46 ± 8.00),(53.72 ± 9.15),respectively,all P ＜ 0.05] ; the protein levels in the control group(100.00 ± 3.86)％ detected by Western blotting were significantly increased in the cortex of rat brains treated with fluoride in both the small and the large amount of fluoride exposure groups[(189.47 ± 3.14)％,(191.36 ± 11.09)％,respectively,all P ＜ 0.05].The significantly increased expression of NF-κB at the protein level was observed in the cortex of rat brains of the small and the large amount of fluoride exposure groups[(365.97 ± 6.04)％ and (417.15 ± 10.89)％,respectively] as compared with the control group[(100.00 ± 10.07)％,all P ＜ 0.05].The mRMA level of P-gp in the cortex of rat brains of the small and the large amount of fluoride exposure groups(2396 ± 427,3479 ± 371,respectively) were higher than that of the control group(260 ± 106,all P ＜ 0.05).Conclusion The increased expressions of P-gp and NF-κB in the cortex of rat brains are induced by chronic fluorosis,which might be connected with the mechanism of brain damages.

ObjectiveTo investigate the transcriptional changes of nitochondria fission and fusion gene loci and reactive oxygen species (ROS) level in cortical neurons of rats with chronic fluorosis,and to reveal their roles in mitochondria damage due to chronic fluorosis.MethodsSD rats were fed with different doses of fluoride through drinking water[＜ 0.5(control),10,50 mg/L,respectively] for 3 and 6 months.The level of ROS and mRNA contents of mitochondria fission gene loci Drp1/Fis1 and fusion gene locus Mfn1 in the cortical neurons of rat brains were detected with ROS fluorescent probe and real-time PCR,respectively.ResultsAs compared with control group [10.43 ± 5.98,(3.4 ± 0.6) × 103,(8.8 ± 1.4) × 10,(1.2 ± 0.2) × 102] at the experiment period of 3 months,the level of ROS and mRNA contents of mitochondria fusion gene locus Mfn1 and fission gene loci Drp1/Fis1 in the cortical neurons were obviously increased in the rats fed with 50 mg/L fluoride through drinking water[25.48 ± 6.09,(1.0 ± 0.2) × 1011,(3.0 ± 1.6) × 103,(8.9 ± 3.6) × 102,all P ＜ 0.05],whereas no significant changes were found in the rats fed with 10 mg/L fluoride[11.67 ± 3.49,(3.1 ± 0.3) × 104,(6.7 ± 2.7) × 10,(5.0 ± 0.9) × 10,all P ＞0.05].Furthermore,at 6 months of the experiment the increases in ROS level(63.02 ± 8.15,65.60 ± 7.40) and mRNA contents of mitochondria fission gene loci Drp1/Fis1 [(2.0 ± 0.8) × 106,(4.0 ± 0.6) × 105,(3.8 ± 1.3) × 103,(1.3 ± 0.2) × 103] and the decrease in mitochondrial fusion gene locus Mfn1[(3.0 ± 0.4) × 106、(4.0 ± 0.9) × 104]were observed in the cortical neurons of the rats fed with 10 mg/L and 50 mg/L fluoride as compared with the control group[25.26 ± 6.41,(3.0 ± 0.8) × 109,(5.1 ± 0.8) × 103,(2.8 ± 0.7) × 102,all P ＜ 0.05].Conclusions Excessive intake of fluorine leads to elevated ROS levels,and decreased transcription of mitochondrial fusion gene loci Mfn1,which is positively correlated with the time and dose-exposed to fluoride.The changes of mitochondrial fission and fusion gene loci in the cortical neurons may be related to high level of oxidative stress induced by chronic fluorosis.

Objective To investigate the deletion pattern of 4.8 kb mitochondrial DNA(mito-DNA) in liver,kidney,and brain of rats with chronic fluorosis and to explore the significance of mitochondria in the pathogenesis of chronic fluorosis.Methods Sixty SD rats were randomly divided into 3 groups according to body mass (20 in each group):control,low-fluoride and high-fluoride groups,and they were fed with different concentrations of fluoride in drinking water (0,10,50 mg/L,respectively) for 6 months.Mito-DNA in liver,kidney and brain was detected by real-time PCR.Results The amounts of 4.8 kb mito-DNA in liver(2.1 × 10-3,1.6 × 10-3),kidney (1.7 × 10-3,1.4 × 10-4) and brain cortex (1.5 × 10-5,1.3 × 10-5) in low-and high-fluoride groups were significantly reduced,as compared with that of control group (2.9 × 10-3,2.0 × 10-3,1.1 × 10-4,all P ＜ 0.05).The amount of 4.8 kb mito-DNA in kidney in high-fluoride group was lower than that in low-fluoride group (P ＜ 0.05).Conclusions Excessive fluoride intake can result in missing of 4.8 kb mito-DNA in liver,kidney and brain cortex.The abnormal of mito-DNA might be related to the dysfunction of mitochondrial respiratory chain.

OBJECTIVE: To establish a multiplex STR genotyping method for autosomal STR and Y-STR loci in forensic biological practice. METHODS: Widely used autosomal STR loci and Y-STR loci were selected. A set of PCR primers was designed, and a 5-dye fluorescent labeled STR multiplex PCR reagent kit was developed. RESULTS: A kit was developed which can simultaneously detect 15 autosomal STR loci, 10 Y-STR loci, and an Amelogenin. CONCLUSION The 15 autosomal STR plus 10 Y-STR kit in combination with capillary electrophoresis method was used to STR genotyping with accurate and reliable results. The new one-step testing kit can potentially be widely used in forensic cases and DNA databank in the future.
Amelogenin ; Chromosomes, Human, Y/genetics* ; DNA Primers ; Databases, Nucleic Acid ; Forensic Genetics/methods* ; Genotype ; Genotyping Techniques/instrumentation* ; Humans ; Indicators and Reagents ; Microsatellite Repeats ; Multiplex Polymerase Chain Reaction

Objective:To evaluate the effect of mechanical chest compression device in patients with cardiac arrest.Methods:The relevant literatures about mechanical cardiopulmonary resuscitation and manual cardiopulmonary resuscitation were systematically searched from China Knowledge Network (CNKI), VIP, Wanfang, PubMed, Web of Science and other databases. The effective data were extracted and analyzed by RevMan5.3 software.Results:A total of 20 clinical studies involving 29 727 patients were included, of which 11 104 patients received mechanical cardiopulmonary resuscitation and 18 623 patients received traditional manual cardiopulmonary resuscitation. The results of meta-analysis showed that mechanical cardiopulmonary resuscitation could not effectively improve the restoration of spontaneous circulation (ROSC) rate, admission survival rate, discharge survival rate and neurological prognosis in patients with cardiac arrest compared with manual cardiopulmonary resuscitation. ROSC occurrence rate ( RR=1.10, 95% CI: 0.99-1.23, P<0.01), admission survival rate ( RR=1.01, 95% CI: 0.95-1.08, P=0.67), discharge survival rate ( RR=1.00, 95% CI: 0.86-1.15, P=0.14), and good neurological function rate ( RR=0.81, 95% CI: 0.61-1.06, P=0.69) showed no significant differences between the mechanical cardiopulmonary resuscitation and manual cardiopulmonary resuscitation. Conclusions:Mechanical chest compression device has no advantage compared with manual cardiopulmonary resuscitation. Mechanical cardiopulmonary resuscitation is not recommended to completely replace manual chest compression in cardiopulmonary resuscitation.