Objective　To investigate the activation of human T cells with superantigen SEA. Methods　T cells proliferation, IL-2 production, DNA synthesis, cell phenotype and apoptosis induced by the SEA in the first or restimulation were detected. Results　 It was shown that 100 ng/mL was the optimal activation concentration, IL-2 production arrived at top level in the third day, SEA activated CD4+ and CD8+T with the same degree, T cells start apoptosis in response to SEA restimulation within 24 hours and apoptosis disappeared through addition of rhIL-2. Conclusions　 There were correlation between activation and SEA concentration or stimulation period； SEA activated both CD4+ and CD8+T cells without change the cell phenotype.

Objective To establish the normal data of the fetal thorax,and to evaluate its values in the diagnosis of fetal thorax malformation.Methods Totally 398 normal singleton fetuses at 16 to 36 gestational weeks(GW) were enrolled,2D-US and 3D-US VOCAL technique were used to measure the 2D data and 3D volumes on the transverse section at the level of the four-chamber view,and the correlation among all measurements with GW was analyzed.Thirty fetuses collected randomly were examined to analyze the reliability.Nine fetuses with congenital thoracic dysplasia (CTD) and 10 fetuses with congenital diaphragmatic hernia (CDH) were assessed and compared with the normal fetuses.Results ① In healthy controls,the fetal thoracic 2D measurements and 3D volumes increased along with the growth of the GW.The regression equations were listed as follows:thoracic transverse diameter (cm) =-0.002 GW2 + 0.301 GW-1.510;thoracic anteroposterior diameter (cm) =0.003GW2 + 0.046GW + 0.666;thoracic area (cm2) =0.071GW2-1.466 GW + 14.728;thoracic circumference (cm) =0.01GW2 + 0.313GW + 3.341;thoracic volume (cm3) =0.285 GW2-7.797GW + 66.592;lung volume (cm3) =0.178 GW2-5.317GW + 45.539;the ratio of lung volume to thoracic volume =0.005GW + 0.396.② The reliabilities of the data obtained by the same/two different operators were good.③ CTD group was obviously lower than the healthy controls in all thoracic measurements (all P ＜0.01).There was no statistical difference in the 2D data between the CDH group and healthy controls (P ＞0.05),while the 3D volumes and the ratio of lung volume to thoracic volume were obviously lower than those in the healthy controls (P ＜0.01).Conclusions 2D-US can evaluate the fetal thoracic development and malformation preliminarily,but 3D-US VOCAL technology plays an important role in distinguishing different types of thoracic malformations.

Objective:To explore the relationship between transcription factor AP 1 and NF kappaB and IL 2 decrease in anergic T cells.Methods:Nuclear proteins of activated T cells and anergic T cells were extracted and then the expression of AP 1 and NF kappaB were determinated by gel electrophorotic mobility shift assay.Results:Compared to activated T cells,anergic T cells expressed defective AP 1 transcription factor;there were three forms NF kappaB complex in both activated T cells and agergic T cells,but NF kappaB transcription activity was higher in anergic T cells than that in activated T cells.Conclusion:It has been demonstrated that these alteration of transcription factors have been likely to be responsible for repression of IL 2 in anergic T cells.

Objective To analyze the expression of dystrophin associated glycoprotein complex (DGC) in Duchnne muscular dystrophy (DMD) in different age groups. Methods The confirmed 24 DMD patients were divided into 3 groups according to their chronological age (children whose age between 1 to 3 were assigned to early childhood group; children whose age between 3 to 6 were assigned to preschool group; children whose age between 6 to 13 were assigned to school-age group). Several proteins from sarcolemmal muscle membrane were analyzed by immunohistocbemistry. Results The primary loss of dystrophin may lead to a secondary or completely deficiency of α-SG, β-SG, γ-SG,δ-SG, β-DG and dysferlin from sarcolemmal muscle membrane in different age groups. The expression of nNOS is completely deficient in the 3 groups, while the expression of caveolin-3 increased. Conclusions The expression of dystrophin related DGC proteins from DMD patients in different age groups showed diversed degrees of deficiency or complete deficiency. The deficiency of these proteins may occur during the embryonic period, while the increased expression of eaveolin-3 may have a relation with the regeneration of skeletal muscle fibers.

Objective To evaluate the effects of dexmedetomidine pretreatment on extracellular sig?nal?regulated kinase ( ERK) pathway during acute lung injury in a rat model of liver transplantation. Meth?ods Sixty male Sprague?Dawley rats, weighing 235-250 g, were divided into 4 groups ( n=15 each) u?sing a random number table: sham operation group (group S), liver transplantation group (group LT), low?dose dexmedetomidine pretreatment group ( group LD ) and high?dose dexmedetomidine pretreatment group ( group HD) . In LT, LD and HD groups, the model of orthotopic liver transplantation was estab?lished, and the operation time was about 4 h. Dexmedetomidine 2?5 and 5?0μg·kg-1 ·h-1 were intrave?nously infused for 1 h starting from 1 h prior to clipping the hepatic artery and portal vein in LD and HD groups, respectively. The rats were sacrificed after the end of operation, and the lungs were removed for determination of wet to dry weight ratio ( W∕D ratio) , cell apoptosis and expression of ERK mRNA, ERK, phosphorylated ERK ( p?ERK) , Bcl?2 and Bax in lung tissues and for examination of the pathological chan?ges ( with light microscope) and ultrastructure of lung tissues ( with transmission electron microscope) . The
injured alveolus rate ( IAR) , apoptosis index ( AI) and ratio of Bcl?2 to Bax expression ( Bcl?2∕Bax ratio) were calculated. Results Compared to group S, the W∕D ratio, IAR, AI, expression of ERK?1 mRNA, ERK?2 mRNA, p?ERK, Bcl?2 and Bax and Bcl?2∕Bax ratio were significantly increased in LT, LD and HD groups ( P<0?05) . Compared to group LT, the W∕D ratio, IAR and AI were significantly decreased, the expression of ERK?1 mRNA, ERK?2 mRNA, p?ERK and Bcl?2 and Bcl?2∕Bax ratio were significantly increased, and the expression of Bax was significantly down?regulated in LD and HD groups (P<0?05). Compared to group LD, the W∕D ratio, IAR and AI were significantly decreased, the expression of ERK?1 mRNA, ERK?2 mRNA, p?ERK and Bcl?2 and Bcl?2∕Bax ratio were significantly increased, and the ex?pression of Bax was significantly down?regulated in group HD ( P<0?05) . The pathological changes of lung tissues were significantly attenuated in LD and HD groups as compared with group LT, and in group HD as compared with group LD. Conclusion The mechanism by which dexmedetomidine pretreatment mitigates cell apoptosis during acute lung injury is related to activation of ERK pathway in a rat model of liver trans?plantation.

Objective To evaluate the effect of penehyclidine hydrochloride on the damage to the non-ventilated lung in the pediatric patients undergoing one-lung ventilation (OLV).Methods One hundred and twenty pediatric patients of both sexes,aged 2-6 yr,with body mass index of 17-24 kg/m2,of American Society of Anesthesiologists physical status Ⅰ or lⅡ and New York Heart Association class Ⅰ or Ⅱ,undergoing elective lobectomy performed via video-assisted thoracoscope,were randomly divided into 2 groups (n=60 each) using a random number table:control group (group C) and penehyclidine hydrochloride group (group P).At 10 rmin before anesthesia induction,penehyclidine hydrochloride 0.05 mg/kg was injected intravenously in group P,and the equal volume of normal saline was given in group C.At 5 min after drug intervention (T0),immediately after onset of OLV (T1),at 60 min of OLV (T2),immediately after the end of OLV (T3),at the end of surgery (T4),and at 24 h after surgery (T5),venous blood samples were collected for determination of serum tumor necrosis factor-alpha (TNF-o),interleukin-6 (IL-6) and IL-8 concentrations by enzyme-linked immunosorbent assay.The specimens of normal lung tissues around the lung lobe to be resected were obtained at T1 and T3 for determination of the injured alveolus count (with a light microscope) and cell apoptosis (using TUNEL) and for examination of the ultrastructure of epithelial cells (with a transmission electron microscope).The injured alveolus rate (IAR) and apoptosis index (AI) were calculated.Results Compared to the value at T0,the IAR and AI were significantly increased at T3,the serum TNF-α,IL-6 and IL-8 concentrations were significantly increased at T2-5 (P＜0.05),and the pathological changes were obvious in the two groups.Compared to group C,the IAR and AI were significantly decreased at T3,the serum TNF-α,IL-6 and IL-8 concentrations were significantly decreased at T2-5 (P＜0.05),and the pathological changes were significantly reduced in group P.Conclusion Penehyclidine hydrochloride can attenuate the damage to the non-ventilated lung in the pediatric patients undergoing OLV,and the mechanism is probably related to inhibition of systemic inflammatory responses and cell apoptosis in lung tissues.

Bone turnover is regulated by local concentrations of cytokines such as osteoprotegerin (OPG) and receptor activator of nuclear factor kappaB ligand (RANKL). To explore the in vivo biological function of Opg and the mechanism of osteoporosis due to deficiency of Opg, Opg knockout mice have been generated through homologous recombination. Opg-/- mice exhibit a sharply decrease in bone density and strength as expected. The number of osteoclasts in Opg-/- mice significantly increases. Morphologically, osteoclasts appear more cuboidal in shape in Opg-/- mice than those of wt mice, suggesting that active osteoclastogenesis occurs in the absence of Opg. In consistent with this finding, an increase of osteoblast activity was also observed with accelerated mineral accumulation rate by histomorphometric measurement and elevated serum alkaline phosphatase activity (ALP) in Opg-/- mice. Interestingly, more than 50% of 2-month-old Opg-/- mice manifest medial calcification of aorta with comparable serum concentrations of calcium and phosphorus to wt mice. In conclusion, Opg-/- mice have a high-bone-rurnover type osteoporosis. The aortic calcification in Opg-/- mice is not due to abnormality of calcium and phosphorus metabolism. The mechanism underlying aortic calcification in Opg-/- mice needs to be further investigated.

Objective To observe the effect of raloxifene, a selective estrogen receptor modulator, on osteoporosis in the osteoprotegerin (OPG) gene knock-out female and male mice. Methods Two groups of OPG gene deficient (OPG-/-) female and male mice, 20 mice in each group, were assigned to raloxifene-treated (3 mg The effect of raloxifene was evaluated by comparing the values of bone mineral density (BMD) , bone strength,histomorphometric measurement and osteoclast number between the raloxifene treated group and placebo group.Results As compared with placebo group osteoporotic manifestations were improved in OPG-/- female mice treated with raloxifene orally. BMD was increased both in lumbar vertebrae (P<0.05) and femurs (P<0.01).Bone strength was measured in femurs by three-point bending test and vertebrae by stress test. Results showed that ultimate load, ultimate stress and Young's modulus were increased both at lumbar and femur bone, suggesting decreased risk of fracture. Tartrate-resistant acid phosphatase, a marker enzyme of osteoclasts, was detected, and the number of osteoclasts declined significantly after the treatment of raloxifene. At the same time, results of histomorphometric measurements indicated that bone trabecular volume was increased and bone formation rate decreased from(8.05±4.02)mm3·mm-2·year-1 to (5.48±1.89)mm3·mm-2· year-1(P＜0.05).These findings were found in the group of OPG-/- female mice treated with reloxifene but not in male mice. Conclusions Raloxifene is effective in treating osteoporosis in female OPG-/- mice, indicating that its action is at least in part independent of OPG gene. But it is ineffective in male OPG-/- mice.

Objective To evaluate the effect of ulinastatin on postoperative outcomes in elderly patients undergoing thoracoscopic radical operation for lung cancer.Methods Sixty patients of both sexes,aged 65-80 yr,weighing 40-85 kg,of American Society Anesthesiologists physical status Ⅱ or Ⅲ,scheduled for thoracoscopic radical operation for lung cancer,were divided into 2 groups (n =30 each) using a random number table method:ulinastatin group (group UTI) and normal saline group (group NS).Ulinastatin 0.5× 104 U/kg was intravenously infused within 1 h before skin incision in group UTI,while the equal volume of normal saline was given instead in group NS.Central venous blood samples were collected at 30 min before skin incision (T0),30 min after start of surgery (T1),and 1 h and 1,3 and 5 days after surgery (T2-5) for determination of the expression of CD42a+,HLADR+ and CD14+ in monocytes (using the flow cytometry),plasma concentrations of interleukin-6 (IL-6),IL-8 and tumor necrosis factoralpha (TNF-α) (by enzyme-linked immunosorbent assay),and the plasma C-reactive protein (CRP) concentration (by immunoturbidimetry).The ratios of monocyte-platelet adhesion (CD42a+/CD14+) and monocyte activation function (HLADR+/CD14+) were calculated.Cognitive function was assessed and scored on day 1 before operation and day 7 after operation,and the incidence of postoperative cognitive dysfunction (POCD) was calculated using Z score.Results Compared with group NS,the CD42a+/CD14+ ratio was significantly decreased at T1-3,the HLADR+/CD14+ ratio was increased at T3,4,the concentrations of plasma IL-6,IL-8,TNF-α and CRP were decreased at T1-5,and the incidence of POCD was decreased in group UTI (P＜0.05).Compared with the baseline value at T0,the HLADR+/CD14+ ratio was significantly decreased at T2-4 in group UTI,the HLADR+/CD14+ ratio was decreased at T2-5,and the CD42a+/CD14+ ratio was increased at T1,2 and T4,5 in group NS,and the concentrations of plasma IL-6,IL-8,TNF-α and CRP were increased at T1-5 in the two groups (P＜0.05).Conclusion Ulinastatin can promote postoperative outcomes in the elderly patients undergoing thoracoscopic radical operation for lung cancer.

Objective: To evaluate the effect of penehyclidine hydrochloride (PHC) on Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling pathway in non-ventilated lung injury in the patients undergoing radical operation for lung cancer. Methods: A total of 100 patients, aged 40-64 yr, with body mass index 18-27 kg/m², of American Society of Anesthesiology physical status Ⅱ or Ⅲ, undergoing radical operation for lung cancer, were divided into 2 groups (n=50 each) according to the random number table method: control group (group C) and PHC group.PHC 0.01 mg/kg was intravenously injected at 10 min before anesthesia induction in group PHC, while the equal volume of normal saline was given instead in group C. The peripheral tissues of the removed lung tissues were obtained for determination of wet/dry weight ratio (W/D ratio). The pathological changes and ultrastructure of lung tissues were observed under light microscope, and lung injury was assessed and scored.The expression of TLR4 and NF-κB protein and mRNA was detected by Western blot and real-time polymerase chain reaction, respectively.Before administration (T₀), at the onset of one-lung ventilation (T₁), at 60 min of one-lung ventilation (T₂), immediately after the end of one-lung ventilation (T₃), at the end of operation (T₄) and at 24 h after operation (T₅), blood samples were collected from the internal jugular vein for determination of serum tumor necrosis factor-alpha, interleukin-6 (IL-6) and IL-8 concentrations by enzyme-linked immunosorbent assay. Results: Compared with group C, the W/D ratio and lung injury scores were significantly decreased, the expression of TLR4 and NF-κВ protein and mRNA was down-regulated, and the concentrations of tumor necrosis factor-alpha, IL-6 and IL-8 were decreased at T₂-T₅ in group PHC (P<0.05). The pathological changes and damage to ultrastructure of lung tissues were significantly attenuated in group PHC as compared with group C. Conclusion The mechanism by which PHC attenuates non-ventilated lung injury is related to blocking TLR4/NF-κВ signaling pathway and reducing inflammatory responses in the patients undergoing radical operation for lung cancer.