Objective To explore the role of IL-1β in inhalation injury repairment through its effects on the expression of prostaglandin E_2 in cultured airway fibroblasts of mouse. Methods The cultured airway fibroblasts in vivo from male Kunming species mouse were randomly divided into control group and treatment group. The superna-rant and cells were collected at different time after treated with IL-1β. The expressions of PGE_2, COX-2 and mPGES1 protein in supernatant and cells were measured by ELISA and Western Blot. Results ①PGE_2 levels in the cultured airway fibroblast supematant at 8 h(148.2±28.3) ng/L,16 h(267.6±45.4)ng/L,24 h(210.5±38.6) ng/L and 48 h(198.7±36.5) ng/L were higher than that in the control group (P < 0.01), and peaked at 16 h;COX-2 ex-pressions at 8 h(0.478±0.029) COX-2/β-actin, 16 h(0.672±0.047) COX-2/β-actin,24 h(0.617±0.036) COX-2/β-antin, and 48 h (0.593±0.034) COX-2/β-actin were higher than that in control group (P < 0.01), and peaked at 16 h;mPGES1 at 8 h(0.300±0.018) mPGES1/β-actin, 16 h(0.549±0.034) mPGES1/β-actin, 24 h (0.497±0.030)mPGES1/β-actin and 48 h(0.443±0.026)mPGES1/β-actin were higher than that in the control group(P < 0.01), and peaked at 16 h. ②PGE_2 in 0.1 μg/L IL-1β group (142.9±2.3) ng/L, 1.0 μg/L IL-1β group (267.6±45.4) ng/L and 10.0 μg/L IL-1β group (587.3±106.9) ng/L were higher than those in the control group (58.5±16.0) ng/L (P < 0.01), and there was significant difference among the three groups (P < 0.01);COX-2 in 0.1 μg/L IL-1β group(0.525±0.031) COX-2/β-actin, 1.0 μg/L IL-1β group(0.672±0.047) COX-2/ β-actin and 10.0 μg/L IL-1β group(1.012±0.064)COX-2/β-actin were higher than that in the control group (0.309±0.019) COX-2/β-actin (P < 0.01), and there was difference among the three groups (P < 0.01);mPG-ES1 in 0.1 μg/L IL-1β group(0.380±0.021) mPGES1/β-actin, 1.0 μg/L IL-1β group (0.549±0.034) mPG-ES1/β-actin, and 10.0 μg/L IL-1β group(0.879±0.045) mPGES1/β-actin were higher than those in the control group(0.199±0.012)(P<0.01),and there was difference among the three groups(P<0.01).Conclusions IL-1β may upregulate PGE_2, COX-2 and mPGES1 expressions in airway fibroblast, indicating that IL-1β influences PGE_2 synthesis through COX-2 and mPGES1 expression and participates in airway inhalation injury course. Airway fibroblasts may be a main source cell of inflammatory mediators in injury repair.

Acute Disease ; Adult ; Angioplasty, Balloon, Coronary ; adverse effects ; Humans ; Hypopituitarism ; etiology ; therapy ; Male

Electrocardiography ; Humans ; Myocardial Ischemia ; physiopathology

Objective To evaluate the efficacy of Cobalt 60 radiotherapy in patients with stage I and II non small cell lung cancer. Methods From March 1977 to December 1992, 63 patients with stage I and II non small cell lung cancer were treated. According to the 1997 UICC staging system, 7 patients had stage IA disease, 10 stage IB, 5 stage IIA, and 41 stage IIB. Forty nine patients were confirmed by histopathology, and 14 cases by cytopathology. Fifty eight patients had squamous cell carcinoma, 3 adenocarcinoma, and 2 mixed squamous cell and adenocarcinama. All patients were treated by Cobalt 60. Patients would receive 40 Gy plus a boost of 15～30 Gy. The total dose was D T55～70 Gy in 6～12 weeks. All patients were followed for more than five years. Results The overall 5 year survival for all patients was 17.5%. Fifty eight (92%) patients have died and 11 survived. For the 58 succumbed patients, 52 (90%) died of tumor, and 26 (45%) of them from local failure. Four patients (7%) died of other causes. Conclusion Radiotherapy is an effective treatment option for non small cell lung cancer.

Objective To investigate the safety and feasibility of electrocoagulation of gallbladder artery in laparoscopic cholecystectomy ( LC) . Methods A total of 376 patients with gallbladder benign diseases underwent LC in our hospital from May 2004 to September 2013.The gallbladder artery was treated by electrocoagulation . Results Because of unclear gallbladder triangle due to abdominal adhesion , conversion to laparotomy was performed in 9 patients.In the remaining 367 patients, three-port LC with electrocoagulation of the gallbladder artery was conducted successfully .Laparoscopic appendectomy was conducted simultaneously in 12 patients.An additional fenestration and drainage of the left renal cyst was performed in 1 patient.Postoperatively, a secondary bile duct exploration was conducted in 1 patient because of bile duct obstruction caused by common bile duct stones . Conclusion The electrocoagulation of gallbladder artery is safe and feasible in LC for the treatment of gallbladder benign diseases .

Objectives To analysis the expression difference of eIF4E in bone marrow between the acute myeloid leukemia (AML) and the non-tumor patient,before and after induction therapy,and the different subtypes of AML,and to explore the relation between eIF4E and other molecular biology abnormalities in AML.Methods The bone marrow specimens of newly diagnosed AML and non-tumor control patients were collected.The expression level of eIF4E was detected by RT-PCR.Results The positive rate of eIF4E was 65.2 ％ (101/155) in AML.eIF4E turned to negative in 12 patients (17.6 ％) who got complete remission after induction therapy.eIF4E was negatively expressed in bone marrow of the nontumor control patients.The positive rates of eIF4E were 75.0 ％ (15/20) and 80.8 ％ (21/26) in M4 and M5 type AML,respectively,and was 59.6 ％ (65/109) in other subtype AML (P ＞ 0.05).FLT3/ITD gene mutation was found in 26 cases of newly diagnosed AML.The eIF4E expression and FLT3-ITD gene mutation were independent each other (P ＞ 0.05).Conclusions eIF4E is positive in most of the newly diagnosed AML and turns to negative in part of AML achieving complete remission.The expression of eIF4E is no difference among different subtype of AMLs.eIF4E and FLT3-ITD gene mutation are independent each other.

Aim To study the effect of PLC on rabbit and human platelet actin polymerization, and then to explore the mechanism of PLC anti-aggregation to platelet. Methods Platelets of rabbit and human were treated with PSS, ASA and different doses of PLC respectively and then were extracted by Triton abstraction. The relative concentration of actin of differently treated platelets induced by ADP was determined by SDS-PAGE and spectrophotometre. Results For rabbit platelets were treated with PSS, the relative concentration of actin determined at static state was 1.682?0.319; when the platelets were treated with ASA 668 ?mol?L -1,PLC 5,10,15,20 and 25 U?ml -1, the relative concentration of actin determined at activated state induced by ADP was 2.450?0.562,1.089?0.322,1.727?0.442,1.450?0.324,1.161?0.306, 0.857?0.242 and 0.692?0.187 respectively. Compared with PSS, inhibition rates (%) of ASA 668 ?mol?L -1, PLC 5, 10, 15, 20, 25 U?ml -1 to the relative concentration of actin were 55.55,29.51, 40.82,52.61, 65.02,71.76 respectively.For human platelets were treated with PSS, the relative concentration of actin determined at static state was 1.358?0.376; when the platelets were treated with ASA 668 ?mol?L -1,PLC 5,10,15,20 and 25 U?ml -1, the relative concentration of actin determined at activated state induced by ADP was 2.445?0.750, 1.096?0.344, 1.705?0.507,1.437?0.416, 1.165?0.355, 0.845?0.257 and 0.679?0.198 respectively. Compared with PSS, inhibition rates (%) of ASA 668 ?mol?L -1, PLC 5, 10, 15, 20, 25 U?ml -1 to the relative concentration of actin were 55.17,30.27, 41.23,52.35, 65.44, 72.23 respectively. Conclusion PLC has significant effects on actin polymerization of rabbit and healthy human platelets (P

Objective: To investigate the effects of low molecular weight heparin(LMWH) on vascular endothelial growth factor(VEGF) expression of early diabetic nephropathy. Methods: Ninety-five male SD rats were randomly divided into three groups: normal control rats, STZ-induced diabetic rats and diabetic rats treated with LMWH. The renal tissues were subjected to immunohistochemical staining after 1,2,4,6,and 8 weeks’ treatment respectively to quantify the VEGF expression. Results: Immunohistochemical staining demonstrated an increasing in VEGF positive cells in diabetic rats. It was found that there were significant differences in VEGF staining intensity between diabetic rats and normal control rats and between LMWH treated rats and untreated diabetic rats after two weeks treatment. Conclusion: The inhibition of VEGF expression may be one of the mechanisms of LMWH’s renal protective effects on early diabetic nephropathy.