Objective To investigate possible intracellular s ignal molecules involved in TGF-?-induced airway smooth muscle cell proli feration in rats. Methods The cultured airway smooth muscle cells were divide d into 3 groups: control group (20 mL?L -1FCS/DMEM), 10 ?g?L -1 TGF-?1 group and 10?g?L -1 TGF-?1 /U-0126 (1 ? mol?L -1) group. The proliferation of ASMCs was detected by MTT. Exp ression of phospho-p42/p44 extracellular signal-regulated kinase (ERKs) with i mmunocytochemistry were examined in different groups. A values were detected by image analysis. Results By MTT, A values of 10?g?L -1 TGF- ?1 group (0.36?0.043) were significantly higher than those of control grou p (0.126?0.052, t=5.44,7.62, P

AIM: To observe the effect of aminoguanidine (AG) on hemodynamics and lung capillary permeability in acute lung injury (ALI) in rabbits. METHODS: 24 rabbits were equally divided into four groups: saline group, endotoxin group, AG group and AG plus endotoxin group. In AG plus endotoxin group, endotoxin was injected to animals to make an ALI model, 25mg/kg AG was injected following that and let this sustain 3 hours. Meanwhile, mean arterial pressure (MAP), mean pulmonary arterial pressures (MPAP) and blood gas analyses were observed during this period. At the end of the experiment, broncho-alveolus lavage was performed, pathologic samples were treated routinely and lung wet weight/dry weight ratio was calculated. RESULTS: After endotoxin injection, MAP and arterial oxygen pressure (PaO 2) decreased, and MPAP increased significantly. The injection of AG had little effect on MAP, but AG could markedly decrease MPAP and increase PaO 2. Cell count in broncho-alveolus lavage fluid (BALF) was less in AG plus endotoxin group than in endotoxin group. Although AG did not affect total protein in BALF, low molecular weight proteins decreased in AG plus endotoxin group by the assay of electrophoresis. Tissue wet weight/dry weight ratio also decreased in this group. Pathologic study showed that there were fewer inflammatory cells and less lung edema in AG plus endotoxin group. CONCLUSION: AG could improve hemodynamics status and attenuate acute lung injury induced by endotoxin in rabbits. [

The vitamin B 12 Productivity of 14 marine bacterial strains isolated from the China Sea was determined microbiologically using Escherichia coli 113 3. Tests were made on the culturing media and culture conditions for Vitamin B 12 production. The results showed that the culturing medium in which the extract from soybean cake with seawater and some nutriments were added was suitable to recognize further some marine Vitamin B 12 producing bacterial strains. The medium with appropriate cobalt chloride and some salts added may be useful for Vitamin B 12 biosynthesis. The PH value of the fermentation for the testing strains was raised with the lapse of time for fermentation. A better Vitamin B 12 production may be obtained by keeping the fermentation liquid slightly basic till about 96h. No.2627 strain in all the strains tested showed well in the productivity. The mixed cultivation of some strains (including No.2627 strain) tested often has potentiality and superiority for Vitamin B 12 production.

Objective To study the apoptosis of endothelial cells and the relation between it and the expression of P53 protein after focal cerebral ischemia reperfusion in rats.Methods The apoptosis of endothelial cell 2,6,12 h and 1,2,3,7,14,21 d after cerebral ischemic reperfusion were observed using an in situ end labeling method,and the expression of P53 protein was detected by immunohistochemical staining methods.Results Apoptotic endothelial cells in ischemic penumbra were observed 2h after cerebral ischemic reperfusion, they peaked at 12~24 h, and decreased gradually.There was no remarkable difference between it and the sham operative group at 21 d.The P53 protein began to express 6h after cerebral ischemic reperfusion, it peaked at 1~2 d, and then declined gradually to controlled level at 7d. The expression peak time of P53 was 24 h later than that of cell apoptosis.Conclusion Apoptosis was a pattern of endothelial cell death after reperfusion of MCAO. P53 protein played an important role in the process of apoptosis of endothelial cells.

AIM: To investigate the relationship between inflammatory cell infiltration and proto-oncogenes expression in asthma. METHODS: Guinea pigs were used as asthma models challenged by ovoglobulin. Dot-blot, Northern-blot and immunochemical techniques were used to detect the expression of c-fos, c-myc, c-jun and c-sis. Inflammatory cell infiltration was showed by pathologic study.RESULTS: c-fos and c-myc mRNA could not be detected or expressed at very low level in control group. Those were greatly increased after the animals are challenged by ovoglobulin. Immunochemical study showed that Fos, Myc, Jun and Sis expressed at low level in control group, and those were increased after the challenge. There was little inflammatory cell infiltration in control group. Lymphocyte, neutrophil and eosinophil were detected immediately after the challenge, a great number of inflammation cells could be seen after 12-24 h of the challenge. Majority of neutrophil and eosinophil were under mucosa or in epithelium in airway. CONCLUSION: Oncogenes expression had strong relationship with airway inflammation.

Objective To separate NK cells of mice from NK cell separation medium and study inhibitory effect of proliferated NK cell induced by low dose radiation on the leukemia model of K562 cells.Methods Flow cytometry and 3H-TdR methods were respectively used to measure proliferation index and activity of NK cells treated with low-dose radiation( which means exposure dose in 20 cGy low LET beam or 5 cGy high LET beam).CD13 + cells were measured by flow cytometry and TNF-α content in blood-serum was detected by ELISA.In vivo,peripheral blood leucocyte count,index of liver,indexes of spleen and kidney were observed in control group and experimental group.Results The purity of NK cell separation was (82.54 ± 0.18)%.The proliferation index of NK cells at 24 hours after 80 mGy irradiated was 36.31 ± 1.32% ,(t =24.69,P ＜0.05).Killing activity of NK cell induced by low dose radiation to K562 cell was (12.59±0.63)%(t=6.63,P＜0.05)and the inhibition ratio was 29.52%.Conclusion The injection of proliferated NK cell induced by low dose radiation demonstrated significant inhibitory effect on the growth of leukemia nude mouse.

Background and purpose: Sorafenib hepatocellular carcinoma assessment randomized protocol (SHARP) and sorafenib in patients in Asia-Pacific region with hepatocellular carcinoma (ORIENTAL) had indicated that multi-kinase inhibitor sorafenib could prolong overall survival (OS) and time to progression (TTP) as well as improve progress free survival (PFS) in patients with advanced stage hepatocellular carcinoma. Drug-related adverse events in the course of treatment restricted its clinical application to a certain degree. This study was aimed to summerize the adverse events as well as the management of sorafenib in our clinic. Methods: Twenty-five cases clinically diagnosed as advanced hepatocellular carcinoma were enrolled from January 2008 to October 2009. All the patients who received sorafenib treatment met inclusion criteria as followed: (1) Progression of disease after trans-hepatic arterial chemoembolization therapy; (2) Extensive portal vein cancerous thrombus formation; (3) Portal zone or retroperitoneal lymph node metastasis or multiple remote metastasis, such as lung or bone; (4) Diffused poor blood supply to tumor; (5) Inform consent was obtained. All adverse events with different grade were observed during the beginning 12 weeks, and clinical treatment were carried out relatively. Results: Total of 25 cases were enrolled. Nine patients died of the disease, 3 of them died during the first 12 weeks, 3 patients abandoned sorafenib treatment, among them 2 died before the finish of 12 weeks treatment and 1 patient discontinued 5 months after the sorafenib treatment. Twenty cases finally assigned. Number of patients encountered drug-related adverse events were: HFSR (hand-foot-skin-reaction) 4(4/20), diarrhea 4(4/20), alopecia 5(5/20), rasb 4(4/20), fatigue 8(8/20), leukopenia and Thrombocytopenia 4(4/20), elevated blood pressure 1(1/20) and abdominal pain 1(1/20). After clinical management, 20 patients' sorafenib treatment were eventually not affected by adverse events. Conclusion: Sorafenib was well-tolerated and is a safe option of treatment for patients with advanced hepatocellular carcinoma.

Objective The purpose of this study is to investigate the apoptosis mechanisms of glioblasto-ma cell line U87 induced by sodium cantharidinate ( SCA) in vitro.Methods Growth inhibition of U87 by 0.625μg/mL,1.25μg/mL,2.5μg/mL,5μg/mL SCA at 24 h,48 h,72 h were analyzed by MTT assay respec-tively.Morphological changes of U 87 nuclear were detected by fluorescence microscope .U87 cell apoptosis and cell cycle arrest were detected after SCA treatment for 24 h and 48 h by flow cytometry.The changes of apoptosis-related genes Bcl -2,Bax,Caspase-3 expression were analyzed after 24 h of SCA treatment by RT -PCR as-say.Results MTT assay showed that growth inhibition of U 87 cell induced by SCA was accompanied with the in-creased drug concentration ,Hoechst33258 staining showed the morphology of apoptotic U 87 cells nucleui ,chromo-some condensation ,nuclear condensation ,some nuclear fragmentation and formation of apoptotic bodies .Flow cy-tometry showed that SCA could induce cell cycle arrest at the G 2/M phase,and could induce apoptosis of U87.RT-PCR results showed that after 24 h of SCA treatment caspase -3,bax expression of U87 was significantly higher than the control group(P<0.05),bcl-2 expression was significantly decreased (P<0.05),and P53 expression was not significantly increased(P>0.05).Conclusion Our results demonstrate that SCA can inhibit U87 pro-liferation and induce apoptosis of U 87 .

Objective: To explore the correlation of left descending anterior (LDA) myocardial bridge (MB) and atherosclerosis at proximal to a segment with MB in patients elderly than 60 years and to identify if LDAMB could become the independent risk factor of atherosclerotic stenosis at proximal to a segment with MB. Methods: A total of 986 patients with multi-slice spiral CT diagnosed coronary artery disease (CAD) were studied and 389 patients with 486 MB in left heart were found. General information as the age, gender, diabetes, hypertension, dyslipidemia and smoking conditions were collected, relationship between LDAMB and atherosclerotic stenosis at proximal to a segment with MB was studied by Logistic regression analysis. Results: There were 48/389 (12.3%) cases with MB at proximal segment of LDA, 254 (65.3%) cases with MB at middle segment of LDA, 51 (13.1%) cases with MB at distal segment of LDA, 19 (4.9%) cases with MB at the ifrst diagonal branch and 17 (4.4%) cases with MB at obtuse marginal branch respectively. Logistic regression analysis presented that age (OR=1.07, 95% CI 0.02-0.09,P<0.01), diabetes (OR=4.48, 95% CI 0.75-2.24,P<0.01) and MB at middle segment of LDA (OR=4.98, 95% CI 0.81-2.41, P<0.01) were related to atherosclerotic stenosis at proximal to a segment with MB; age (OR=1.08, 95% CI 0.04-0.12,P<0.01) and diabetes (OR=3.49, 95% CI 0.30-2.19,P=0.01) were related to the atherosclerosis at LAD middle segment; the MB at LAD middle segment was not related to atherosclerosis of middle and distal LAD segments,P>0.05. Conclusion: MB at middle segment of LDA was with the higher occurrence rate of atherosclerotic stenosis at proximal to a segment with MB in elderly patients, which could be used as an independence risk factor for clinical diagnosis.

AIM: To observe the antiproliferative effect of c-myc antisense oligonucleotide in rat thymus lymphocytes. METHODS: Rat thymus lymphocytes were separated by Ficoll-Urografin density gradient centrifugation. Lipofectin was used to introduce antisense, sense and mismatched oligonucleotides for c-myc to rat thymus lymphocytes. The antiproliferative effect was assayed by incorporation of -TdR and MTS cell proliferation assay. TR-PCR was used to detect the expression of c-myc mRNA. RESULTS: c-myc antisense oligonucleotide inhibited rat thymus lymphocytes proliferation [(0.14?0.03)A vs (0.32?0.16)A, P