To observe the effect and its potential mechanism of monoclonal antibody to tumor necrosis factor-alpha(TNF? MoAb)on systemic hemodynamics and survival rate after intestinal ischemia/reperfusion (Ⅱ/R). Method: SD rats were subjected to 75 rain of superior mesenteric artery occlusion followed by 6 hours of reperfusion. The animals were treated intravenously with either TNF? MoAb(20mg/kg)or the control protein(albumin, 20mg/kg) 30 min prior to the onset of ischemia. Result: Pretreatment with TNF? MoAb significantly attenuated the decrease in blood pressure and cardiac index compared to controls throughout the 6-hour period of observation(P

To evaluate the effect of delayed treatment with monoclonal antibody to tumor necrosis factor-alpha (TNF-? MAb) on systemic hemodynamics and multiple organ dysfunction following prolonged hemorrhagic shock and resuscitation. Method: Adult male Sprague-Dawley rats were subjected to prolonged hemorrhagic shock (MAP of 4.00-4.66 kPa for 180 rain)followed by resuscitation over 50 min. The animals were treated intravenously with either TNF-? MAb (20.0 mg/kg) or the control protein(albumin,20.0 mg/kg)15 rain after the end of resuscitation(65 min after shock). Result: Compared to the albumin controls, delayed treatment with TNF-? MAh significantly reduced the total peripheral resistance index (P

AIM: To research the processed products of Rhizoma Atractylodis Macrocephalae at the level of sesquiterpene lactones from it. METHODS: Sesquiterpene lactones were separated by the silica gel column and layer preparation, and the active substances were determined by HPLC. RESULTS: Atractylone、atractylolide Ⅰ, atractylolide Ⅲ, and biepiasterolid were separated from Rhizoma Atractylodis Macrocephalae. Atractylone was (0.535 8)%, atractylolide Ⅰ was (0.044 0)% and actractylolide Ⅲ was (0.081 4)% in Atractylodis stir-fried with wheat bran determined by HPLC. CONCLUSION: The method has good accuracy and repeatability and it can be used for the quality control of Rhizoma Atractylodis Macrocephalae.

Objective To investigate the effect of nuclear factor-kappa B (NF-?B) signal transcription pathway inhibitor-pyrrolidine dithiocarbamate (PDTC) on mRNA expression of high mobility group box-1 protein (HMGB1) in organs of rats with endotoxic shock and its potential mechanism. Methods Forty-seven male Wistar rats were randomly divided into normal control group (n=8), endotoxic shock group (n=24), and PDTC treatment group (n=15). At serial time points, the animals in each group were sacrificed, and tissue samples from the liver, lungs and kidneys were harvested to determine HMGB1 mRNA expression and pulmonary MPO activity. Also, blood samples were collected to determine the major organ functional indices. Results Compared to normal controls, HMGB1 mRNA levels were significantly increased in samples from the liver, lungs and kidneys at 2-6h after endotoxin challenge (P

Objective To investigate the effect of lipopolysaccharide (LPS) on stimulating high mobility group box-1 protein (HMGB1) mRNA expression in peritoneal macrophages in rats and its potential signaling mechanism. Methods Abdominal macrophages obtained from male Wistar rats were seeded on 24-well (1?10 6 cells/well) tissue culture plates. The cells were incubated for 3 days before they were stimulated with LPS, fludarabine (specific inhibitor of signal transducer and activator of transcription 1, STAT1), or rapamycin (specific inhibitor of signal transducer and activator of transcription 3, STAT3). After being stimulated, macrophages were denatured directly in tissue culture plates to determine HMGB1 mRNA expression. The time-dependent and dose-dependent responses between LPS stimulation and HMGB1 mRNA expression were analyzed, and the effect of treatment with fludarabine and rapamycin on HMGB1 mRNA expression was also observed. Results After being stimulated with 75-100ng/ml LPS, the HMGB1 mRNA expressions in macrophages were up-regulated markedly, peaking at 24-36 hours, and remained elevated up to 48 hours. It was found that the HMGB1 mRNA expression was significantly inhibited by treatment with either fludarabine (100?mol/L) or rapamycin (25ng/ml). Conclusions These data suggest that LPS stimulation can result in up-regulation of HMGB1 mRNA expression in peritoneal macrophages in rats. Janus kinase/STAT pathway may be involved in modulating HMGB1 mRNA expression in LPS-activated macrophages.

Objective:To establish a fluid dynamics model of upper airway before and after surgery and explore the changes of three-dimensional fluid dynamics in patients with micrognathia.Methods:A patient with micrognathia and severe obstructive sleep apnea-hypopnea syndrome(OSAHS)accepted CT scan before and six months after mandibular advancement operation.Computation-al fluid dynamics model was built on the base of CT scan by Mimics 1 0.01 and ANSYS ICEMCFD1 4.0.The internal flow of upper respiratory tract was simulated by ANSYS-FLUENT 1 4.0 and the results were analyzed by Tecplot.Results:Fluid dynamics model of upper airway was constructed before and after the surgery respectively.The volume of the upper airway of the patient increased from 37.284 cm3 to 44.498 cm3;the most narrow area of upper airway was located in the lower bound of pharyngopalatiae,and it was augmented from 1 .1 35 cm2 to 2.297 cm2;the minimum pressure was decreased from1 01 308 Pa to 1 01 272 Pa;the maximum air velocity increased from 3.476 m/s to 4.978 m/s.Conclusion:Mandibular advancement may correct the occlusal deformity,ex-panse the upper respiratory tract,decrease the negative pressure and maintain the patency of the airflow in the treatment of patients with micrognathia and OSAHS.

Objective To investigate costimulatory molecules CD80 and CD86 expression in acute myelogenous leukemic cells and clinical implication.MethodsThe expression of CD80 and CD86 in the patients with acute myelogenous leukemia and HL-60 cells,U937 cells,NB4 cells,K567 cells was confirmed by Flow Cytometer.ResultsCD80 was very low or no expression in patients with acute myelogenous leukemia.CD86 expressed in acute myelogenous leukemia (27.86±19.65)%,which was much higher than that in control group[(1.21±0.13)%,t＝3.55,P＜0.01].No significant changes were observed in the expression of CD86 in M4 cells(48.65±21.92)%,M5 cells(39.25±18.67)% and control group(50.20±20.31)%(P＞0.05).After the cells were cultured for 24 h and 48 h,the expression of CD86 was (30.62±5.35)% and (29.43±4.67)% in HL-60 cells ,(24.12±5.23)% and (26.56±6.54)% in U937 cells,and,(21.25±3.78)% and (23.21±6.98)% in NB4 cells (all P＞0.05).The expression of CD80 and CD86 was very low in K562 cells.ConclusionsCostimulatory molecules CD86 expressed in acute myelogenous leukemic cells in the patients with acute myelogenous leukemia and HL-60 cells,U937 cells,NB4 cells.

Objective To observe the expression of tumor necrosis factor-α induced protein 8 like-2 (TIPE2) in CD4 + CD25 + regulatory T cells ( CD4 + CD25 + Tregs) and analyze its potential effect on immunosuppressive activity of CD4 + CD25 + Tregs. Methods CD4 + CD25 + Tregs were purified from spleen of the BALB/c mice by using magnetic cell sorting system.The expressions of TIPE2 mRNA and protein in CD4 + CD25 + Tregs were detected by using RT-PCR and Western blot.CD4 + CD25 +Tregs were further infected with the recombinant lentiviruses that carried small interference RNA(siRNA)to knock down the TIPE2 expression.Based on the expressions of cell surface molecules including cytotoxic T-lymphocyte-associated antigen (CTLA)-4 and forkhead/winged helix transcription factor p3 (Foxp3) detected by flow cytometry and the levels of cytokines including interleukin (IL)-10 and transforming growth factor (TGF)-3 examined by ELISA in CD4 + CD25 + Tregs,the functional role of TIPE2 in controlling suppressive activity of CD4 + CD25 + Tregs was analyzed.In the meantime,the proliferation activities of T effector cells were assayed by MTT test. Results A 147 bp TTPE2 gene band and a clear TIPE2 band with a molecular mass of approximately 21 000 in CD4 + CD25 + Tregs were detected by using Westem blot.Cell surface molecule as well as cytokine expressions were significantly down-regulated when the CD4 + CD25 + Treg stimulated and activated by anti-CD3/CD28 was cultured for 24 hours after the siRNA silenced CD4 + CD25 + Treg cells ( P ＜ 0.01 ).Meanwhile,the suppression role of CD4 +CD25 + Tregs on the proliferation activity of T effector cells was weakened obviously ( P ＜ 0.05 ). Conclusions As an important immunoregulatory molecule,TIPE2 not only expresses in the CD4 + CD25 +Tregs,but also affects the immunosuppressive function of CD4 + CD25 + Tregs.

Objective To evaluate the radiation dose to patients using radial and femoral artery access in coronary angiography (CAG) and intracoronary stenting (IS) ,provide basis for clinical intervention path .Methods The data of 190 samples (43 by femo-ral and 147 by radial) underwent CAG and 54 samples (17 by femoral and 37 by radial) underwent CAG+IS were analyzed retro-spectively .All samples were divided into two groups (radial group and femoral group) by different approach ,and radiation dose in different approach were analyzed .Results There was no significant difference of Dose Area Product (DAP) and Cumulative Dose (CD) using femoral and radial access in CAG (P>0 .05) .Separating two samples which CD were much higher than others ,the mean DAP was 23 .93 Gy · cm2 and the mean CD was 358 .85 mGy using radial vs .27 .06 Gy · cm2 and 369 .57 mGy using femoral , not distinctive either(P=0 .734 ,P=0 .834) .In CAG+IS ,the mean DAP was 82 .64 Gy · cm2 using radial and it was 78 .11 Gy · cm2 using femoral ,and the mean CD was 1 286 .41 mGy using radial and it was 1 267 .76 mGy using femoral .There were no signifi-cant difference in both DAP and CD (P=0 .705 ,P= 0 .919) .Conclusion The radiation dose of DAP and CD were not different when using radial access and using femoral access in CAG and CAG +IS .

Objective To investigate the effect of the inhibitor SB203580 of p38 mitogen-activated protein kinase (MAPK) signal transduction pathway on biopterin (BH 4)/nitric oxide (NO) expression and elucidate the potential mechanism of MAPK in biopterin-mediated NO induction after endotoxic shock. Methods A total of 56 male Wistar rats were randomly divided into normal control group (n=8), endotoxic shock group (n=32) and SB203580 treatment group (n=16). After animals were sacrificed, tissue samples from the liver, the lungs as well as the kidneys were harvested to determine the expressions of guanosine triphosphate cyclohydrolase I (GTP-CHI) and inducible nitric oxide synthase (iNOS) mRNA and observe the changes of BH 4 and NO levels in blood and tissues. Results With endotoxin challenge, GTP-CHI mRNA expression and BH 4 levels were significantly elevated in various tissues and maintained at high levels up to 24 hours. Similarly, the iNOS mRNA expression and NO levels in the tissues significantly increased too, especially in the liver and the lungs. Treatment with SB203580 significantly down-regulated GTP-CHI mRNA expression in the liver, the lungs and the kidneys at 12, 24 and 2-12 hours, respectively (P