Objective　To examinate the portal system hemo dynamics of portal hypertension in patients with cirrhosis and analysis the rela tionship between the changes of the portal system hemodynamics and the Child-Pu gh grade.Methods　The portal system hemodynamics of portal hypertension we re examined in 100 patients with cirrhosis and 24 normal subjects used colo r Doppler ultrasound and 100 cirrhosis patients were graded by the Child-Pugh g rade.Results　There were significant changes in the portal system hemo dynamics of portal hypertension between cirrhosis and 24 normal subjects,the di ame ter of the portal vein(Dpv),the splenic vein(Dsv) and the superior mesenteric vein(Dsmv), the speed of the portal vein(Vpv),the spleni c vein(Vsv) and the superior mesenteric vein(Vsmv) ,the flow of the portal vein(Qpv),the splenic vein(Qsv) and the superior mesenteric v ein(Qsmv) were significantly increased (P<0.01),respectively.The Dpv of Child grade C patients were wider than the those of Child grade A a nd B patients(P<0.05), the Vpv of Child grade C patients had mo re decrease than the those of Child grade A and B patients(P<0.05), but Qpv was were no significant difference between Child grade A,B and C gro ups patients(P>0.05). Conclusions　Examination of the portal system hemodynamics of por tal hypertension in patients with cirrhosis can be used to evaluate the degree o f liver function and the portal hypertension in cirrhosis patients.

Objective　To investigate the expression of IGF-1 and TGF-β1 at different stages of hypertension in the spontaneously hypertensive rats (SHR) and their relationship with ventricular hypertrophy and myocardial fibrosis in the left ventricle. Methods　The expression of IGF-1 and TGF-β1 mRNA were measured with RT-PCR. Dynamic changes of the left ventricular hypertrophy and myocardial fibrosis were examined by biochemical assay and image analysis. Results　Increased expression of IGF-1 was observed from the 14 th to the 24 th week which coincided with the progress of the left ventricular hypertrophy (LVH), but not with that of myocardial fibrosis (MF). No significant change was observed in the expression of TGF-β1 in SHR group when compared with that of control. Conclusion　Increased expression of IGF-1 in the left ventricle of SHR is probably associated with the progress of LVH.

Aquaporins (AQPs) is a novel family of membrane protein which is in charge of the transportation of water across the membranes. It has been testified that AQPs may be related to many physiological functions and pathophysiological disorders. In lung, 6 subtypes of AQPs were found, 4 of which have been located in certain tissue. AQP1, AQP3, AQP4 and AQP5 are located in upper respiratory tract and may contribute to the mucus production, bronchial moisturizing and gland secretion. AQP1 and AQP5 are located in lower respiratory tract and may participate in directing the water movement across the blood-gas barrier. AQPs in natal lung may be an important factor to accelerate the reabsorption of the lung liquid. In adult, some diseases such as asthma, pulmonary edema, adult respiratory distress syndrome, which have been considered unbalanced water movement, may be also concerned with AQPs. The relationship between lung edema and AQPs have not been elucidated in details. It should be verified how AQPs work in more organs and tissues as well as in some diseases.

Objective To testify the lung injury induced by cardiopulmonary bypass(CPB) in canine model and observe the influence of CPB on the aquaporin-1 ( AQP1 ) mRNA expression in canine lung. Methods 8 mongrel dogs were used to perform the cardiopulmonary bypass. The hearts arrested for 90 minutes with mild hypothermia and rebeated for 6 hours. The hemodynamics, the ratio of lung dry weight and wet weight, the plasmic osmotic pressure, and the characteristics of light and fine structure were analyzed. The retro-transcription polyase chain reaction ( RT-PCR ) was used to measure the expression of AQP1 mRNA during the CPB. Results The hemodynamic data were stable in different time point during the CPB (P ＞0.05 ). The ratio of lung dry weight and wet weight was getting lower ( P ＜0.001) and the plasmic osmotic pressure was getting higher due to the prolongation of the CPB time and reperfusion time ( P ＜0.01). The light and electron microscopy showed the prominent aggregation of the white blood cell, severe interstitial edema and mild tear of respiratory membrane after 3 hour and 6-hour rebeat. AQP1 mRNA expression in lung was downregulated, 78.4% after 3-hour reperfusion and 55.5% after 6-hour reperfusion respectively, comparing to the level before CPB. Conclusion We recognize that the lung injury and lung edema were severe following 3-hour and 6-hour rebeat in CPB and hypothesize that the down-regulation of lung AQP1 mRNA expression may be a sign of pulmonary interstitial capillary injury induced by CPB.

Objective To introduce the technique and efficacy of the treatment of avulsion fracture at tibial insertion of anterior cruciate ligament(ACL) in children through internal fixation by hollow cancellous bone screw under arthroscope.Methods December 2002 ～December 2007,internal fixation using percutaneous reduction by leverage was conducted in 68 children with avulsion fracture at tibial insertion of ACL in our hospital.In 68 children,there were 29 females and 39 males,aged 6～15 years(average age of 12 years),including 22 cases of typeⅡ(with limited knee extension)and 46 cases of type Ⅲ.The fracture was fixed by hollow titanium cancellous bone screw.Results Sixty eight cases were followed up for an average of 18 months(12～36 months).The muscle tension(mea sured by KT-2000) in injured side was recovered close to the uninjured side.Excellent reduction,solid inter nal fixation,complete healing,stable knee joint and negative Lachman and drawer tests were shown in this clinical setting.No swelling,pain and knee dysfunction were found.Impingement sign at intercondylar fossa disappeared.The patients were satisfied with their functional recovery.There was no abnormal angulation and shortness.Conclusion Treatment of avulsion fracture(type Ⅱ with limited knee extension or type Ⅲ) at tibial insertion of ACL by arthroscopic internal fixation with hollow titanium alloy cancellous bone screw could obtain accurate and reliable reduction,and avoide epiphysis injury with satisfactory functional recovery.

Dendritic cells (DC) are antigen presenting cells (APC) that play critical roles in the initiation of T cell response and development of T cell-dependent antibodies in vivo. CD34_+ hematopoietic progenitor cells of bone marrow and peripheral blood can differentiate into DC when cultured with GM-CSF and TNF-? in vitro. In the present study, we cultured monocytes isolated from human peripheral blood with 100ng/ml hGM-CSF and 500U/ml hIL-4 for one week, and then found that a large number of DC with high purity were gengerated. DC expressed MHC I , MHC II and costimuladng moleculers highly on cell surface and cound stimulate proliferation of allogeneic T lymphocytes. Self serum or fetal calf serum are best for generation of DC. When hGM-CSF was used alone, the monocytes differentiated into macrophages but not to DC. TNF-? could induce further maturation of DC when added in late period of the culture. Generation of DC from human peripheral blood may facilitate further studies on DC and their clinical applications.

Objective: To study the effect of different dissolution media on the dissolution curve of risperidone oral soluble films to provide reference for the quality evaluation of the preparation.

Objective To study the protective role against cisplatin-induced ototoxicity by using radix astra-gali in rats. Methods Forty rats were randomly divided into four groups. Group A received saline as controls. Group B received radix astragali. Group C received injection of cisplatin(4 mg/kg) as experiments for 6 days. Group D received both radix astragali (5 g/kg) and cisplatin (4 mg/kg). Distortion product acoustic emission (DPOAE) was applied to each rat before and 7 days after cisplatin injection. All the animals were sacrificed on the 7th day. Half of the cochleas were observed by frozen section and the apoptosis of hair cells was detected by TUNEL meth-od. Scanning electron microscopy was utilized to evaluate the cochlear morphology of the other rats. Results The DPOAE amplitudes of Group C decreased significantly compared to the group A and group B(P<0.01). The dam-age and apoptosis of hair cells were noted in the group C and group D, while the hair cells of group A and group B showed no sign of apoptosis or damage. Compare to experimental group , the DPOAE amplitudes of group D were higher, and the damage and apoptosis of hair cells were significantly lower(P<0.05). Conclusion This study sug-gests that radix astragali can effectively reduce cisp[atin ototoxicity.

Objective To study calcium chelator BAPTA-AM antagonize the cellular oxidative stress induced by hydrogen peroxide ( H2 O2 ) and to explore the effect of calcium ion on the cell degeneration mediated by NLRP3.Methods The SHSY5Y cell model of oxidative stress was made by hydrogen perox-ide,then the cell model was treated with calcium ion carrier A23187 or BAPTA-AM,a higher efficiency cal-cium chelating agent.The cells were divided into 4 groups:H2O2 treatment group,H2O2+A23187 group, H2 O2+A23187 +BAPTA-AM group and control group.NLRP3 protein was detected by Western blot,and Caspase-1 and IL-1βwere detected by ELISA.Results NLRP3 expression was significantly increased in cells treated by hydrogen peroxide(P<0.05) .The NLRP3 protein continued to increase, and the expression of Caspase-1((57.1±19.2)pmol/L) and IL-1β((484.2±49.5)pg/ml) protein was also increased signifi-cantly in cells treated by A23187,and the difference had statistically significant for caspase-1 or IL-1βin H2O2+A23187 group compared with those in control group(Caspase-1:(26.8±12.9)pmol/L,IL-1β:(326.9 ±52.1) pg/ml) (P<0.05, P<0.01) .NLRP3,Caspase-1 and IL-1βwere all significantly reduced after adding a high-er efficiency calcium chelating agent BAPTA-AM.Conclusion Calcium overload is likely to enhance the oxidative stress induced by hydrogen peroxide and engender neurodegeneration mediated by NLRP3 inflammasome.