Objective To evaluate catheterization in pancreatic duct before endoscopic papillary bal-loon dilation (EPBD)to prevent pancreatitis after EPBD.Methods Forty-three patients with normal serum amylase levels,diagnosed as having bile duct stones,underwent EPBD.Twenty-three were assigned to experi-mental group,where catheters(ERCP imaging tube)were placed in pancreatic duct before EPBD,then the pa-pillary balloon was expanded to 10 mm.Twenty were assigned to control group where eight-millimeter-diameter papillary balloon was used to remove the stones.The serum amylase levels before EPBD,6 hours and 24 hours after EPBD,the incidence of pancreatitis and high serum amylase levels associated with EPBD,as well as the mean time and success rate of removing the stones of the two groups were compared.Results Post-EPBD pan-creatitis occurred in one patient in experimental group (4.35%),and seven in control group (35.00%), which was significantly different(P <0.05).Meanwhile,the mean levels of serum amylase 6 h and 24 h after EPBD in the experimental group were (102.61 ±98.99)U /L and (60.35 ±26.18)U /L respectively,lower than those in the control group (398.25 ±259.32)U /L and (230.50 ±281.31)U /L(P <0.05).After the papillary balloon was expanded to 10 mm in experimental group,the mean time of removing stones was (10.43 ±2.27)min,which was shorter than that of control group (17.90 ±4.49)min (P <0.05).Stone-re-moving rate of two groups had no difference and they all succeeded one time.Conclusion Placing catheter in pancreatic duct before EPBD to prevent pancreatitis after EPBD makes it easier to remove stones in shorter op-eration time.It can prevent pancreatitis and high amylase blood disease after EPBD.

BACKGROUND:Now researches on psychiatric disease and molecular heredity are becoming more and more gradually because of the development of molecular genetics,but conclusions are controversial,and for the time being there are no reports about whether there are regional differences and ethnical differences in the distribution of genotype frequency of 5-hydroxytryptamine 2A receptor gene T102C.OBJECTIVE:Researches on the geographic distribution of genotype frequency of 5-hydroxytryptamine 2A receptor gene T102C of schizophrenics people.DESIGN:Sample survey and observation with schizophrenics selected as subjects.SETTING: Mental Department, Changzhou Peace Hospital.PARTICIPANTS: The experiment was completed in The No.102 Hospital of PLA from January 1999 to August 2003.Totally 177 people of Han nationality (Age: 18-45; Duration of illness: 1 month-20 years) from different provinces and autonomous regions of China in compliance with diagnostic standards of Psychiatric Disease Classification and Diagnosis Standards of China (The 3rd version) were selected as the subjects.METHODS:The blood samples from 117 schizophrenics were given test of polymerase chain reaction(PCR),and the distribution differences of genotype frequency of 5-hydroxytryptamine receptor gene of normal control population from different provinces and autonomous regions were compared. DNA were abstracted by means of phenol chloroform, amplification and cataphoresis test of polymerase chain reaction of target DNA,primer sequence of gene segment amplification of 5-hydroxytryptamine (5-HT) 2A receptor gene T102C: 5'-TCT GCT ACA AGT TCT GGC TT-3', 5 '-CTG CAG CTT TTT CTC TAG GG-3'; Reaction system of 50 μL, DNA 0.5 μg,Primer 50 pmol,TagDNA enzyme 2U were added with dNTP to the final concentration of 200 μmol/L.MAINOUTCOMEMEASURES: DNA cataphores is test of schiophrenicanddistributionofgenotypefrequencyof5-hydroxytryptamine 2A receptor gene.RESULTS: The distribution of genotype frequency of 5-hydroxytryptamine(5-HT) 2A receptor gene: A1A1, 0.07-0.03; A1A2, 0.50-0.72; A2A2,0.17-0.29. Correlation analysis of genotype frequency in different regions:A1A1, x2=4.44, P=0.617 1, P ＞ 0.05;A1A2, x2=1.14, P=0.942 2, P ＞ 0.05;A2A2, x2=0.93, P=0.985 7, P ＞ 0.05.CONCLUSION: The geographic distributions of genotype frequency of 5-hydroxytryptamine 2A receptor gene T102C of schizophrenics of the Chinese Han nationality people were comparatively even.

OBJECTIVE: To investigate the protective effects of dexmedetomidine (DEX) against cerebral ischemia/reperfusion (I/R) injury in mice and its relation with mitochondrial fusion and fission. METHODS: Male ICR mice were randomly divided into sham-operated group, I/R group, I/R+DEX group and I/R+DEX+dorsomorphin group. Mouse models of cerebral I/R injury were established by modified thread occlusion of the middle cerebral artery. DEX (50 μg/kg) was injected intraperitoneally at 30 min before cerebral ischemia, which lasted for 1 h followed by reperfusion for 24 h. The neurobehavioral deficits of the mice were evaluated based on Longa's scores. The volume of cerebral infarction was detected by TTC staining. The changes in mitochondrial morphology of the brain cells were observed with transmission electron microscopy. Western blotting was performed to detect the expressions of phosphorylated AMP-activated protein kinase (p-AMPK), mitochondrial fusion protein (Mfn2) and mitochondrial fission protein (p-Drp1) in the brain tissues. RESULTS: DEX pretreatment significantly reduced the neurobehavioral score and the percent volume of cerebral infarction in mice with cerebral I/R injury. Treatment with dorsomorphin (an AMPK inhibitor) in addition to DEX significantly increased the neurobehavioral score and the percent volume of cerebral infarction in the mouse models. Transmission electron microscopy showed that DEX obviously reduced mitochondrial damage caused by cerebral I/R injury and restored mitochondrial morphology of the brain cells, and such effects were abolished by dorsomorphin treatment. Western blotting showed that DEX pretreatment significantly increased the expressions of p-AMPK and Mfn2 protein and decreased the expression of p-Drp1 protein in the brain tissue of the mice, and these changes were also reversed by dorsomorphin treatment. CONCLUSIONS Preconditioning with DEX produces protective effects against cerebral I/R injury in mice possibly by activating AMPK signaling to regulate mitochondrial fusion and fission in the brain cells.
Animals ; Brain Ischemia ; Dexmedetomidine ; Male ; Mice ; Mice, Inbred ICR ; Mitochondrial Dynamics ; Reperfusion Injury