Objective To provide high-quality health care services to persons whose access is restricted by geography or environment and disaster or battle situation. Methods X-ray equipment was based on embedded Linux operating system, and used OMAP1510 as its hardware developing platform. Telemedicine image workstation was based on Windows operating system, and used VC++6.0 as its software developing platform. Results Telemedicine image workstation could achieve and process images from X -ray machine. Conclusion The system can be applied to real-time acquisition of medical images and telemedicine.

Medical image equipment is used not only to research the structure and principle of imaging equipment but to train the students′ ability of analyzing and solving problems. In order to improve the experiment teaching, simulation devices and practice matches are all involved in.

Objective To investigate the effect of dexmedetomidine on protein kinase RNA-like endoplasmic reticulum kinase (PERK) signaling pathway in cardiomyocytes of the rats with severe scald.Methods Twenty-four healthy adult male Sprague-Dawley rats,weighing 220-280 g,were randomly divided into 3 groups (n =8 each) using a random number table:control group (group C),severe scald group (group S),and scald + dexmedetomidine group (group D).Thirty percent of the total body surface area was shaved on the back and then exposed to 94 ℃ water for 12 s to establish the model of 3rd degree scald.Dexmedetomidine 30 μg/kg (2 μg/ml) was intraperitoneally injected immediately after scald in group D.Myocardial specimens were obtained at 12 h after scald for examination of the pathological changes and for determination of cell apoptosis and expression of C/EBP-homologous protein (CHOP),PERK,and phosphorylated PERK (p-PERK) by Western blot.The apoptosis index and p-PERK/PERK ratio were calculated.Results Compared with group C,the apoptosis index was significantly increased,the expression of CHOP,PERK and p-PERK was significantly up-regulated,and the p-PERK/PERK ratio was significantly increased in S and D groups (P＜0.05).Compared with group S,the apoptosis index was significantly decreased,the expression of CHOP,PERK and p-PERK was significantly down-regulated,and the p-PERK/PERK ratio was significantly decreased (P＜0.05),and the pathological changes of myocardium were significantly attenuated in group D.Conclusion The mechanism by which dexmedetomidine inhibits apoptosis in cardiomyocytes is related to inhibition of PERK signaling pathway in the rats with severe scald.

Objective To evaluate the effects of remifentanil post-conditioning on aquaporin-1 (AQP-1) expression during myocardial ischemia-reperfusion (I/R) injury in rats.Methods Twenty-four male.SpragueDawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =8 each) using a random number table:sham operation group (group S),group I/R,and remifentanil post-conditioning group (group RP).Myocardial I/R was induced by 45 min occlusion of left anterior descending branch of coronary artery followed by 24 h reperfusion.Remifentanil 10 μg· kg-1· min-1 was infused over 10 min starting from 10 min before reperfusion in group RP,while the equal volume of normal saline was given instead in S and I/R groups.At the end of reperfusion,all the rats were sacrificed and their myocardial specimens from left ventricles were obtained for microscopic examination of thepathological changes and for determination of AQP-1 mRNA (using real-time fluorescent quantitative PC R) and AQP-1 protein (by Western blot) expression in the ischemic area and myocardial water content.Results Compared with S group,myocardial water content was significantly increased in the other two groups,AQP-1 mRNA and protein expression was up-regulated in group I/R,and no significant change was found in AQP-1 mRNA and protein expression in RP group.Compared with I/R group,myocardial water content was significantly reduced,and AQP-1 mRNA and protein expression was down-regulated in RP group.Conclusion Remifentanil post-conditioning reduces myocardial I/R injury possibly through down-regulating AQP-1 expression in myocardial tissues of rats.

Objective 　To assess the association between the gene of complement C4A, C4B deficiency and schizophrenia. Methods　192 patients with schizophrenia and 142 healthy controls were tested with the amplification restriction fragment length polymorphism (Amp-RFLP) technique.Results　The frequency of C4AQ0/C4AQ0 homozygote was higher in the patient group than in the control group (χ2=8.54, P＜0.01). The relative risk (RR) of C4AQ0/C4AQ0 homozygote for schizophrenia was 6.8. There was no increased frequency of C4B deficiency in patients with schizophrenia (χ2=0.11, P＞0.05, RR=0.73).Conclusions　These results indicate that there is a positive association between complement C4A dificiency and schizophrenia. Moreover, our study did not support a widespread association between a deficiency in complement component C4B and schizophrenia.

ObjectiveTo investigate the effects of sevoflurane anesthesia on aquaporin-9 (AQP-9) expression in brain tissue after focal cerebral ischemia-reperfusion (I/R) in rats.MethodsSeventy-five male SD rats weighing 230-270 g were randomly divided into 3 groups ( n =25 each):group sham operation (group S) ; group I/R and group sevoflurane anesthesia (group SE).All the animals were tracheally intubated under 2.0％ sevoflurane and mechanically ventilated.Anesthesia was maintained with fentanyl infusion at 25 μg· kg-1 · h-1 after a bolus of fentanyl 10 μg/kg and inhalation of 65％ N2O in O2 in groups S and I/R and with inhalation of 2％ sevoflurane in 35％ O2 in group SE.Focal cerebral ischemin was induced by occlusion of middle cerebral artery for 2 h using a nylon thread with rounded tip which was inserted into the right internal carotid artery and advanced cranially until resistance was met.The neurologic function was assessed and scored (0=no deficit,4 =unable to move,unconscious) and brain edema rate (volume of ischemic hemisphere-volume of contralateral hemisphere ÷volume of contralateral hemisphere × 100％ ) and expression of AQP-9 were determined at 6 h,1,2,3 and 5 d of reperfusion.ResultsFocal cerebral I/R significantly increased neurologic deficit scores,brain edema rate and AQP-9 expression in brain tissue in group I/R as compared with group S.Sevoflurane anesthesia significantly attenuated the I/R-induced increase in neurologic deficit scores and brain edema rate and further increased I/R-induced increase in AQP-9 expression in brain tissue.ConclusionSevoflurane anesthesia can reduce focal cerebral I/R injury by up-regulating the expression of AQP-9 in brain tissue.

Objective To evaluate the effect of acute hypervolemic hemodilution (AHH) on myocardial damage in severely burned rabbits.Methods Eighteen healthy adult rabbits,weighing 2.0-2.5 kg,were randomly divided into 3 groups (n =6 each) using a random number table:control group (group C),burn group (B group) and AHH group.Rabbits were subjected to 3rd degree burn covering 40％ of the total body surface area.After the model was established,6％ hydroxyethyl starch 130/0.4 was infused intravenously,and the target Hct was 25％ in AHH group.Before AHH (To) and at 2,4 and 8 h after AHH (T1-3),left ventricular systolic pressure (LVSP),left ventricular end-diastolic pressure (LVEDP),+dp/dtmax and-dp/dtmax were recorded,and blood samples from femoral veins were taken to determine the concentration of serum cardiac troponin I (cTnI) by ELISA.The rabbits were sacrificed at T3,and myocardial specimens were removed for microscopic examination of pathological changes with light microscope.Results Compared with group C,the serum cTnI concentration and LVEDP were significantly increased,LVSP and +dp/dtmaxwere decreased at T1-3 in B and AHH groups,and-dp/dtmax at T1-3 in group B and-dp/dtmax at T3 in group AHH were decreased.Compared with group B,LVSP,+dp/dtmax and-dp/dtm,x were significantly increased at T1-3,and no significant change was found in serum cTnI concentration and LVEDP in group AHH.There was no significant difference in the pathological changes between group B and group AHH.Conclusion AHH can not aggravate the early myocardial damage in severely burned rabbits.

Objeetlve To avoid inserting the tip of the central venous catheter into internal jugular vein (IJV) through subclavian vein under ultrasound guidance.Methods sixty breast cancel patients aged 28-63 yr weighing 41-70 kg who needed long-term intravenous infusion and chemotherapy through central venous catheter were randomly divided into 2 groups (n=30 each):control group (group C) and ultrasound group (group U).In group C the insertion of central venous catheter through subclavian vein was guided by pulsatile injection of ice-cold saline.In group U ultrasound detector (type HFL 38/13-6 MH,Sonosite Co,USA) was used to guide the insertion of tbe central vesons catheter.The position of the catheter tip was verified by X-ray radiography.The rate of successful placement at 1st attempt was calculated.Results The tip of the central venous catheter was correctly placed in the vena cava and right atrium in all patients in group U (success rate 100%),while in group C the tip was misplaced in IJV in 6 patients (success rate 80%) and had to be replaced.Conclusion Ultrasound guidance is effective for correct placement of the tip of central venous catheter in the vema cava and right atrium through subclavian vein.

Objective To evaluate the changes in the expression of spinal aquaporin-4 (AQP4) during remifentanil-induced hyperalgesia in a mouse model of incisional pain.Methods Seventy-two pathogen-free healthy adult male CD1 mice,weighing 25-30 g,were divided into 4 groups (n=18 each) using a random number table:control group (group C),incisional pain (group I),remifentanil group (group R) and remifentanil plus incisional pain group (group R+I).Normal saline was infused subcutaneously in group C.An incision was made in the left hind paw in group I.Remifentanil 80 μg/kg was subcutaneously infused for 30 min at a rate of 0.8 ml/h in group R.Remifentanil was infused subcutaneously before establishment of the model in group R+I.The thermal paw withdrawal latency (TWL) and mechanical paw withdrawal threshold (MWT) were measured at 1 day before establishment of the model (T0) and 6 h and 1,2 and 7 days after establishment of the model (T1-4).After measurement of the pain threshold at T3,12 animals were sacrificed randomly,and the lumbar segment of the spinal cord was removed for determination of the distribution and expression of AQP4 by Western blot.Results Compared with group C,the TWL was significantly shortened at T1-3,and the MWT was decreased at T2-4 in R and R + I groups,and the expression of AQP4 was significantly up-regulated at T3 in I,R and R+I groups (P＜0.05).Compared with group I,the TWL was significantly shortened at T2,3,and the MWT was decreased at T2.4 in group R,and the TWL was significantly shortened at T1-3,the MWT was decreased at T2.4,and the expression of AQP4 was up-regulated at T3 in group R+I (P＜0.05).Conclusion The mechanism by which remifentanil induces hyperalgesia is related to up-regulation of AQP4 expression in the spinal cord in a mouse model of incisional pain.