Orphan nuclear receptor steroidogenic factor 1 (SF-1) is a member of the nuclear receptor superfamily. It regulates the expression of multiple genes involved in adrenal and gonadal development,steroidogenesis,and reproductive function. Twenty five different mutations have been described and their clinical features are various. Detection of SF-1 gene may be contribute to the etiological diagnosis for 46, XY disorder of sex development patients.

fulminant liver failure(FLF)is a rapid onset life-threatening emerency in which liver dysfunction,liver failure and hepatic encephalopathy occur within 8 weeks in previouslv norillal person.It has been confirmed by available clinical experience and literatures during the past decades that FLF patients are ideal recipients of liver transplantation.However,the prognosis of the FLF patients who accepted liver transplantation differed greatly according to the available reports because of the differences of supportive treatment during waiting period,the criterion for recipient assessment,the determination of operation chance,the use of critical techniques during operation and postoperative management between different transplantation centers.We probe the standardized clinical use of the aspects above mentioned in liver transplantation for FLF,particularly discuss the treatment of complications resulting from coagulopathy,determination of operation chance,significance of standardized etiological treatment and the indication of the use of veno-venous bypass technique during transplantation to provide better treatment strategy and improve the prognosis of FLF patients.

Randomly divide the said patients into 2 groups,32 cases in treatment group treated with head skin and abdominal acupuncture,body acupuncture for the control group of 28 cases.The result shows the cure rate is 56.25% for treatment group,37.5% for control group.By comparison,P

0.05).Both femur bone lengths in 3.2mm group were shorter than those in the 1.5 mm and 2.2 mm groups.No abnormalities of cartilage cells were observed,without obvious histological evidence of inflammation;only nonspecific foreign body reaction and macrophage infiltration were noticed.Conclusion: PDLLA rod itself does not cause any disturbance to the development of the epiphyseal plate.The growth disturbance of epiphyseal plate depends on the area of injured epiphyseal plate;a injured area over 7% of epiphyseal plate may cause the growth disturbance of epiphyseal plate.

Cumene Hydroperoxide(CHP)-induced mouse mitochondrial lipid peroxides (LPO) are significantly higher than those of the normal mitochondria ( P

Male mice were subjected to 6 Gy total body irradiation,20% TBSA full thickness burns,or both the injuries respectively,and then lipid peroxides (LPO),vitamin E,sulfhydryl groups,respiratory control ratio (RCR),ADP/O ratio,and cytochrome oxidase activity of hepatic mitochondria were determined in the animals in the first 9 postinjury days.It was found that.1.LPO level increased in the early postinjury stage in the combined radiation-burn injury group.2.Vitamin E level decreased significantly in both the groups with either only irradiation or burns.3.The sulfhydryl groups showed a tendency to increase in all the 3 groups.4.The activity of cytochrome oxidase increased signficantly on the 7th postinjury day in the combined injury group.5.RCR and ADP/O ratios decreased more significantly in the combined injury group than in either the single injury group.These facts suggest that the suppression of the respiratory function of hepatic mitochondria results from the damage of mitochondrial membranes due to iipid peroxidation.

The fatty acid content of liver mitochondria was quantitatively determinde with gas chromatography in rats after they were inflicted with 15% TBSA full thickness burns or after the liver mitochondria were incubated with lipids extracted from eschar tissue(D1)or from normal skin of rats(D'1).It was found that after burn injury,the content of unsaturated fatty acid of liver mitochondria decreased and that of saturated fatty acid increased significantly.Both Dl and D'l decreased the content of unsaturated fatty acid and the decrease would be more significant when the concentration of eschar lipids or skin lipids was increased.D1 reduced the unsaturated fatty acid content more significant than D'1 when the two were in same concentration.The possible mechanism of the decrease of unsaturated fatty acid in the liver mitochondria induced with burn injury,eschar lipids or normal skin lipids was discussed briefly.

The effects of tetrandrine on serum TXB2, 6 - Keto - PGF1?, LPO and lipids in patients(n= 40)with essential hypertension has been studied. The results showed that: (1) The levels of serum 6 - Keto -PGF1?,apoA1 in EHT were lower and the level of serum TXB2,LPO and apoB100 were higher than those in control. (2)Patients with essential hypertension treated with tetrandrine (0.1 ~ 0. 2g,tid,po)for 3 mon revealed that thelevels of TXB2, LPO and apoB100 were decreased, and the levels of apoA1 and 6 - Keto - PGF1? were increased. In conslusion,tetrandrine stimulated the synthesis of PGI2 and inhibited the release of TXA2 and normalized the metabolism of lipids in patients with essential hypertension.

Objective To study the effect of remifentanil precondition on myocardium against ischemia/ reperfusion (I/R) injury. Methods Fifty male SD rats weighing 300-350 g were anesthetized with intraperitoneal 5% pentobarbital 40 mg?kg-1, tracheostomized and mechanically ventilated. Right carotid artery and jugular vein were cannulated for BP monitoring and drug administration. ECG, BP and HR were monitored continuously. The chest was opened and heart exposed via a left thoracotomy. A 6-0 prolene suture was placed around the left coronary artery and a snare was made. The coronary artery was occluded by tightening the snare. Myocardial ischemia was confirmed by the appearance of a regional cyanosis of myocardium, decrease in BP and ST-T changes on ECG. After the surgical procedure a 15-minute stabilization period was allowed. The animals were then randomly divided into 3 groups: Ⅰ control group (CON, n = 9) ; Ⅱ ischemic preconditioning group (IPC, n = 9) and Ⅲ remifentanil preconditioning group which was further divided into 5 subgroups according to the dose of remifentanil (RPC) . In control group the hearts were subjected to 30 min ischemia followed by 120 min reperfusion (I/R). In IPC group the hearts were subjected to 3 episodes of 5 min ischemia in succession at 5 min interval for reperfusion before I/R. In RPC group the animals received 3 periods of 5 min remifentanil infusion at 0.2 (RPC1 , n = 5), 0.6 (RPC2,n = 6), 2 (RPC3 ,n = 8), 6 (RPC4 ,n = 7) or 20 (RPC5 ,n = 6) ?g?kg-1?min-1 at 5 min interval before I/R. MAP, HR and RPP (SP?HR) were recorded before and after I/R. Infarct size (IS) and the area at risk (AAR) were determined by triphenyltetrazolium staining. Results MAP was significantly lower at the end of 30 min ischemia in RPC2, RPC3, RPC4 and RPC5 subgroups than in control group. There was no significant difference in MAP, HR and RPP at the end of 120 min reperfusion among the 3 groups. The infarct size was significantly smaller in IPC and RPC groups than in control group. RPC at 6 ?g?kg-1?min-1 provided best protective effect. The sigmoidal equation of the dose-effect curve was Y = 15.18 + 17.76/ [1 + 10(-2.57-X)]. ED50, was 2.689 ?g?kg-1?min-1.Conclusion Remifentanil and IPC have similar protective effect on the heart against I/R injury.

Lipid extract of burn eschar (D_1) added to isolated rat liver mitochondrialcaused depression of respiratory control ratio (RCR), ADP/O ratio, rate of ATP produc-tion, respiration rate in state 3 but it stimulated the respiration rate in state 4. Pretreat-ment with vitamin E significantly prevented the inhibition of mitochondrial respiratoryfunction caused by D_1. The addition of vitamin E after that of D_1 had no protective ef-fect. Heat-treatment of D_1 markedly reduced its inhibitory effect on mitochondrial respira-tory function. Cumene hydroperoxide (CHP) markedly depressed mitochondrial respiration.Vitamin E caused a significant increase in RCR, which was inhibited by CHP at lowerconcentrations. Vitamin E reduced MDA formation considerably in normal mitochondriaand in those mitochondria incubated with D_1, heated D_1 or CHP. These findings indicatedthat D_1 -and CHP-induced depression of mitochondrial respiratory function was probablydue to lipid peroxidation damage which was proved by the protective effct of the pota-tive antioxidant vitamin E.