Objective To study the relationship between magnesium level in umbilical vein and mother′s peripheral blood with intrauterine growth retardation (IUGR) and fetal weight. Methods 39 pregnant women with IUGR were randomly divided into 3 groups: Group 1 (n= 14): The patients were treated with 10% glucose 500 ml + danshen compound 14 ml + low molecular weight dextran 500 ml iv; Group 2 (n= 14): in addition to the same treatment as in group 1, 25% magnesium sulfate 20 ml in 5% glucose 500 ml iv was given; Group 3 (n= 11): no treatment was given; and another 12 normal term delivery women were served as control. Magnesium concentration levels were determined in both maternal peripheral blood and their fetal umbilical vein. Results Maternal serum magnesium level was higher in Group 2 (1 06?0 09) mmol/L than that in Group 1 (0 69?0 05) mmol/L (P

0.05). Chuansu Jiuxin Capsule could improve haemorheology (mainly act on blood viscosity, plasma viscosity and HCT), degrade platelet function (increase TXB2 level and decrease 6-keto-PGF1? level) and protect endothelia (increase ET and decrease NO level). Conclusions Chuansu Jiuxin Capsule was effective and safe for the treatment on AP patients with syndrome of blood stasis in collateral of heart.

Objective To investigate the association of uncoupling protein 2 ( UCP-2 ) gene promoter -866G＞A polymorphism and ischemic stroke in diabetic patients.Methods A total of 844 type 2 diabetic patients including 404 cases with ischemic stroke and 440 cases without ischemic stroke were selected for the 4 year prospective study,Genomic DNA was extracted from the whole blood samples of subjects,UCP-2 gene promoter -866G ＞ A polymorphism was detected by TaqMan MGB probe method,and then the genotype and allele gene frequencies were compared.Results The risk of ischemic stroke in type 2 diabetic female patients with AA+GA genotypes of UCP-2 was higher than that with GG genotype (P＜0.05),but there was no difference among male patients with three genotypes.Conclusions UCP-2 gene promoter -866G ＞ A polymorphism increases the risk of ischemic stroke in Chinese diabetic women.

Objective To observe the effect of dexmedetomidine on plasma SDF-1 level in in hepatic portal occlusion operation.Methods Fifty patients with live cancer undergoing elective partial hepatectomy were selected,no gender limitation,aged 42 to 71,body mass index(BMI) 18.5 ～ 26.0 kg/m2,ASA grade Ⅱ or Ⅲ.The patients were randomly divided into 2 groups(n=25):control group and dexmedetomidine group.The dexmedetomidine group was performed the pump injection of dexmedetomidine 1 μg/kg at 15 min before induction of anesthesia.After induction the rate was changed to 0.4μg · kg-1 · h-1 until 15 min before the end of operation;the control group adopted the same method for conducting continuous intraverous infusion of the same capaci ty of 0.9％ sodium chloride.The peripheral venous blood was collected in 2 groups at preoperative 1 h (T0),postoperative 1 h (T1),postoperative 1 d (T2),postoperative 3 d(T3).The plasma SDF-1 level was detected by using enzyme-linked immunosorbent assay(ELISA).Results There was no statistically significant difference in liver resection range,blood loss,first porta hepatis vessel occlusion time,anesthesia time and plasma SDF-1 level before surgery between the two groups (P＞0.05).Compared with pre-operation,plasma SDF-11evel at T1,T2,T3 time point was significantly increased (P＜0.05).The plasma SDF-1 level at T1,T2,T3 time point in the dexmedetomidine group was lower than that in the control group(P＜0.05).Conclusion SDF-1 expression is significantly increased during perioperative period in the patients with hepatic portal occlusion operation,and intraoperative continuous dexmedetomidine can significantly reduce the SDF-1 level,which inhibits the chemotaxis and accumulation of inflammatory ceils to some extent.

Objective To explore the effect of different cold ischemia (CI)times on the patterns of intra-graft T cell activation gene-3 (TCA-3) expression early after isogeneic half liver transplantation (PLT)in mice. Methods The models of C57BL/6 full-size(FS) and PLT were established.The CI time was 1,4 and 8 h.Specimen were collected at 4 and 24 h post-reperfusion.Ribonuclease protection assays (RPA)was used to evaluate serial mRNA expression of the TCA-3 chemokine in all mice.Histopathology was used to examine cold ischemia injury in the liver grafts. Results A total of 45 control and 30 PLTs were performed.The survival rate at 7 day after control and PLT was 100％.Quantitative analysis demonstrated the levels of TCA-3 mRNA expression were low at 4 h after reperfusion in control group with 1,4,8 h CI.The levels of TCA-3 significandy increased at 4 h after reperfusion in PLT group with CI of 1,4,8 h and the difference between the two groups was statistically significant ( F =7.41,P ＜ 0.05 ). TCA-3 mRNA expression significantly decreased at 24 h after reperfusion in two groups. But the difference was not statistically significant ( P ＞ 0.05 ). Histopathology showed severer cold ischemia injury in PLT grafts compared with control grafts. Conclusions The expression of TCA-3 significandy increased early after PLT and played an important role in cold ischemia injury.TCA-3 could be used as the early therapeutic target for reducing ischemia injury in PLT grafts.

Objective To evaluate the changes in the expression of annexin A2 (ANXA2) in lung tissues in rats with hepato-pulmonary syndrome.Methods Healthy 3-4-month-old Sprague-Dawley rats of both sexes,weighing 220-250 g,were randomly divided into 3 groups:control group (group C,n =10),sham operation group (group S,n =10) and hepatopulmonary syndrome group (group HPS,n =20).The rats were anesthetized with intraperitoneal 3％ pentobarbital sodium 0.1 ml/100 g.Hepatopulmonary syndrome was produced by chronic ligation of the common bile duct.After 5 weeks,the rats were sacrificed and lungs were removed for determination of ANXA2 and smooth muscle actin α (SM-α-actin) mRNA and protein expression in lung tissues by RT-PCR and Western blot,respectively.Results There was no significant difference in the expression of ANXA2 and SM-α-actin mRNA and protein between groups C and S (P ＞ 0.05).The expression of ANXA2 and SM-α-actin mRNA and protein was significantly higher in group HPS than in groups C and S (P ＜ 0.05).Conclusion The expression of ANXA2 in lung tissues is up-regulated in rats with hepato-pulmonary syndrome.

Objective To evaluate the effects of the serum in the patients with obstructive jaundice on the proliferation,migration and phenotype modulation of human pulmonary arterial smooth muscle cells (PASMCs).Methods PASMCs were isolated from the patients,underwent passage and were then subcultured.The cultured PASMCs were incubated with the serum in the patients with obstructive jaundice or with the serum in the healthy volunteers.At 24,48 and 72 h of incubation,the proliferation and migration of the cells were determined by CCK-8 assay and wound healing assay,respectively,and Western blot analysis was used for detection of smooth muscleα-actin (SM-α-actin) and calponin protein expression in human PASMCs.Results The proliferation and migration of human PASMCs were significantly enhanced,calponin protein expression was up-regulated at 24 h of incubation,and the SM-α-actin and calponin protein expression was down-regulated at 48 and 72 h of incubation when human PASMCs were incubated with the serum in the patients with obstructive jaundice as compared with those when the cells were incubated with the serum in the healthy volunteers.When human PASMCs were incubated with the serum in the patients with obstructive jaundice,the proliferation and migration of the cells were significantly enhanced,SM-α-actin expression was up-regulated and calponin protein expression was down-regulated at 48 h of incubation as compared with those at 24 h of incubation.When human PASMCs were incubated with the serum in the patients with obstructive jaundice,the migration of the cells was significantly enhanced,and no significant change was found in the proliferation and SM-α-actin and calponin protein expression at 72 h of incubation as compared with those at 48 h of incubation.Conclusion The serum in the patients with obstructive jaundice can enhance the proliferation and migration of human PASMCs and promotes synthetic PASMC phenotype.

Objective To evaluate the effect of bilirubin on proliferation of pulmonary microvascular endothelial cells (PMVECs) of rats.Methods Primary PMVECs harvested from 10 healthy male Sprague-Dawleyrats,weighing 120-150 g,aged 2-3 months,were cultured,purified and identified.PMVECs were seeded in low-glucose DMEM culture medium or 96-well culture plates,and divided into 5 groups according to the random number table:control group (group C) and different concentrations of bilirubin groups (B1-4 groups) with 30 wells or48 flasks in each group.In group C,low-glucose DMEM 1 ml was added.In B1-4 groups,5,10,20 and 50 μmol/L bilirubin 1 ml were added,respectively.At 24,48 and 72 h of incubation,proliferation of PMVECs was measured using CCK-8 assay and 3 H-TdR incorporation assay,Akt1 mRNA and Smad3 mRNA expression was measured by RT-PCR,and phosphor-Akt1 (p-Akt1) protein and Smad3 protein expression was detected using Western blot.Results Compared with group C,no significant changes were found in each parameter mentioned above at each time point in B1 and B2 groups,the proliferation of PMVECs was weakened,and Akt1 mRNA,p-Akt1 protein and Smad3 protein and mRNA expression was down-regulated at 48 h of incubation in B3 group,and the proliferation of PMVECs was weakened,and the expression of Akt1 mRNA,p-Akt1 protein and Smad3 mRNA and protein was down-regulated at 48 and 72 h of incubation in B4 group.Compared with group B3,the proliferation of PMVECs was weakened,and the expression of Akt1 mRNA,p-Akt1 protein and Smad3 mRNA and protein was down-regulated at 72 h of incubation in B4 group.Conclusion High concentration of bilirubin can inhibit proliferation of PMVECs and down-regulated expression of Akt1 and Smad3 is involved in the mechanism.

Objective To establish a method for culture of rat pulmonary capillary pericytes.Methods Six male Sprague-Dawley rats,aged 6-7 weeks,weighing 200-220 g,were anesthetized and the chest was opened.The pulmonary capillary was isolated by type Ⅰ collagenase digestion and micropore filtration and cultured in highglucose DMEM/F12 1∶1 containing 10％ fetal bovine serum and 0.5％ mixture of penicillin and streptomycin.The morphology and growth of cells were observed with inverted phase contrast microscope.The positive cells of αsmooth muscle actin (α-SMA),desmin,neuron-glial antigen 2 (NG2),cluster of differentiation 31 (CD31) were counted by immunofluorescence.The percentage of positive cells was calculated.Results The microscopic examination showed cells of shuttle shape or star shape,mononuclear cells,binuclear cells occasionally,oval nucleus,rich cell plasma,growth in the shape of vortex or fence,and no contact inhibition.The percentage of positive cells ofα-SMA,desmin,NG2,and CD31 was (99.0± 1.2)％,(96.0±2.1)％,(99.0±0.7)％ and0,respectively.Conclusion The culture method for rat pulmonary capillary pericytes is successfully established.

Objective To investigate the role of serine threonine protein kinase-1 (Akt1) and Smad3 in lung tissues in development of hepatopulmonary syndrome in rats.Methods Seventy-two healthy male SpragueDawley rats,aged 3-4 months,weighing 200-250 g,were randomly divided into 3 groups (n=24 each):control group (C group),sham operation group (S group) and common bile duct ligation (CBDL) group.The rats were anesthetized with 3％ pentobarbital sodium 45 mg/kg.In group CBDL,laparotomy was performed,the common bile duct was ligated and then the abdomen was closed,while the common bile duct was only exposed,but not ligated and then the abdomen was closed in group S.At 1st,3rd and 5th weeks (T1-3),8 rats were chosen randomly in each group and blood samples were obtained from the abdominal aorta for blood gas analysis.The rats were then sacrificed and lungs were isolated to detect the expression of Aktl and Smad3 mRNA and protein in lung tissues (by RT-PCR and Western blot).The lung tissues were sliced and stained with hematoxylin eosin for examination of the pathological changes of pulmonary capillaries.Results Compared with C and S groups,the expression of Akt1 and Smad3 mRNA and protein in lung tissues was significantly up-regulated at T2,3,and alveolar-arterial oxygen tension difference was increased at T3 in CBDL group (P ＜ 0.05).The pulmonary capillary was obviously dilated at T3 in CBDL group.Conclusion The expression of Akt1 and Smad3 in lung tissues is up-regulated,which may be one of the mechanisms of development of hepatopulmonary syndrome in rats.