In order to solve the problems about the lack of investing capital and to evade investing risk,a military hospital can achieve better economic benefit by introducing cooperative medical items.This method can not only make full use of its own good invisible assets and medical resource,but also help to raise its level of medical service and expand its market of medical service.To make a good item of cooperative medical service,special attentions must be payed to the following aspects such as prophase demonstrating,contract signing,partitionning of income and expenditure,financial accouting and daily accouting.

Objective To review the regulation of liver regeneration factors.Methods The literatures about liver regeneration related regulators in recent years were reviewed.Results With further advancement of researches on regulators of liver regeneration in recent years,there were more therapies for treatment of liver-related diseases.Regulators play important roles in the process of liver regeneration,as one of which,cell growth factor plays an essential role in liver cell proliferation,such as the proper expression of TNF-? and IL-6 promoting liver cell proliferation,HGF,TGF-?,EGF,ALR,FS,and others motivating liver cell proliferation,while TGF-? and IL-1 physically terminating liver cell proliferation.Conclusion By strengthening the studies on liver regeneration regulators,new methods may appear for treating liver-related diseases.

Enhancing medical humanistic quality education is the essence of medicine and it is also a necessity of conforming to the transformation of medical model.The pathological teachers should improve their humanistic quality actively,integrate humanistic quality training into pathology teaching and focus on training the social responsibility and healthy psychological qualities in order to enhance medical students' humanistic accomplishment and to make them become high qualified medical talents.

Cardiovascular System ; Forkhead Transcription Factors ; Humans

Objective To observe the role and mechanism of CO-releasing molecules (CORMs) -2in the injured lung induced by ischmia-reperfusion (IR) of hind limbs of rat.Methods The rat model of lung injury was made by ischemia in hind limbs of rat for two hours and then reperfusion for two hours as well.There were 40 SD rats randomly ( random number) divided into 5 groups ( n =8 ),namely sham ischemia-reperfusion (I/R) group,sham I/R + CORM-2 group,I/R group,I/R + CORM-2 group and I/R + DMSO (Dimethylsulfoxide) group. Rats in sham I/R group underwent laparotomy without infrarenal aorta occlusion.The lung tissue structure,polymorphonuclear neutrophil (PMN) count,wet-to-dry weight ratio (W/D), malondialdehyde (MDA) content, myeloperoxidase (MPO) activity, intercellular adhesion molecule-1 ( ICAM-1 ),nuclear IκBα degradation and NF-κB activity in the lung were measured.Results Compared with the sham I/R group,the number of PMNs in lung,W/D,MDA content,MPOactivity,ICAM-1 and NF-κB activity significantly increased in I/R group,whereas nuclear IκBα decreased (P ＜ 0.01).Compared with the I/R group,the number of PMNs in lung,W/D,MDA content,MPO activity and ICAM-1 significantly decreased in I/R + COMR-2 group ( P ＜ 0.01 ), while nuclear IkBαincreased. Conclusions These data demonstrate that CORM-2 attenuates limb I/R-induced lung injury by inhibiting ICAM-1 protein,NF-κB pathway and the leukocytes sequestration in the lung following limb I/R in rats,suggesting that CORM-2 could be used as one of the most valuable therapeutic agents.

AIM: To study the signal pathway involved in up-regulation of LPS-induced HO-1 expression by CCK-8. METHODS: Forty-two SD rats were divided into 7 groups (six rats each) randomly as follows: control group, LPS group, LPS+SP600125 (JNK-specific inhibitor) group, CCK-8+LPS group, CCK-8+LPS+SP600125 group, CCK-8 group and CCK-8 +SP600125 group. Lungs from the rats in these 7 groups were excised 6 h after the agents were administered. HO-1 mRNA expression was examined by RT-PCR. The protein expression of HO-1 was detected by Western blotting and immunofluorescence flow cytometry (FCM). RESULTS: There were significant positive expression of HO-1 mRNA in LPS group compared to control group. CCK-8 enhanced LPS-induced HO-1 mRNA expression and CCK-8 alone induced HO-1 mRNA expression as well. The mRNA expressions of HO-1 in LPS group, CCK-8+LPS group and CCK-8 group were 3.01 (P<0.01), 5.88 (P<0.01) and 3.45 (P<0.01) times as many as that in control group, respectively. SP600125 inhibited the mRNA expression of HO-1 induced by CCK-8 and (or) LPS. The change of HO-1 protein expression was in accordance with that of HO-1 mRNA expression by Western blotting and immunofluorescence FCM. CONCLUSION: These results suggest that JNK/c-Jun signal pathway plays an important role in the up-regulation of LPS-induced HO-1 expression by CCK-8.

AIM: To investigate the role of hydrogen sulfide (H_2S) in the cholecystokinin octapeptide (CCK-8) attenuating lipopolysaccharide (LPS)-induced lung injury. METHODS: A rat model of lung injury induced by intravenous injection of LPS was developed. Male Wistar rats were divided into normal control group, LPS group, LPS+CCK-8 group and CCK-8 group. Six hours after LPS injection, partial pressure of oxygen in the arterial blood (PaO_2), H_2S content and cystathionine-γ-lyase (CSE) activity in lung tissue were detected. The mRNA expression of CSE in lung tissue was determined by RT-PCR;the structure of lung tissues was observed under optical microscope. RESULTS: Compared to normal control rats, the LPS-treated rats had significantly decreased PaO_2 level, increased index of quantitative assessment (IQA) score, while H_2S content, CSE activity and the mRNA expression of CSE in lung tissue were significantly increased (all P<0.05). Administration of CCK-8 into LPS-treated rats increased the PaO_2 level and alleviated the degree of lung injury (measured by IQA score). In addition, CCK-8 decreased H_2S content, CSE activity, and the mRNA expression of CSE (all P<0.05). No significant difference of the above-mentioned parameters between CCK-8 group and normal control group was observed. CONCLUSION: CCK-8 reduces LPS-induced lung injury through inhibiting the generation of endogenous H_2S.

Objective: To study the effects of deguelin on proliferation and apoptosis of human breast cancer cell line MCF-7 and on phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway. Methods: After treatment with 0, 1, 5, 10, 15 and 20 μmol/L of deguelin for 6, 24, 48 and 72 hours, the proliferation inhibition rate of MCF-7 cells was measured by cell counting kit-8 assay. Apoptosis rate of MCF-7 cells was detected with Annexin V-fluorescein isothiocyanate/propidium iodide double staining by flow cytometry and the apoptotic morphology was observed under a transmission electron microscope. After treatment with 0, 1 and 5 μmol/L of deguelin for 6 hours, 5 proteins involved in the PI3K/Akt signaling pathway were examined by Western blot analysis. Results: Deguelin at doses of 5, 10, 15 and 20 μmol/L inhibited the proliferation of MCF-7 cells at 6, 24, 48 and 72 hours. There was a significant difference in each group compared with the control group (P<0.01). The inhibitory effect was more marked with increasing concentration and duration of treatment. There were statistical differences (P<0.05) among 5, 10, 15 and 20 μmol/L groups. However, 1 μmol/L of deguelin had no obvious effects on the proliferation of MCF-7 cells at 6, 24, 48 and 72 hours, showing no significant difference compared with control group (P>0.05). Deguelin at doses of 5, 10, 15 and 20 μmol/L induced apoptosis of MCF-7 cells at 6 hours. There were significant differences (P<0.01) in the early and late apoptosis rate between the treated groups and the control group. The typical apoptotic MCF-7 cells were observed under the transmission electron microscopy. However, 1 μmol/L of deguelin had no apparent effect in inducing apoptosis of MCF-7 cells at 6 hours. After treatment with 5 μmol/L of deguelin for 6 hours the expression of phosphorylated phosphatase and tensin homologue deleted on chromosome 10 (PTEN) (Ser380), phosphorylated 3-phosphoinositide-dependent protein kinase 1 (PDK1) (Ser241), phosphorylated Akt (Thr308) and phosphorylated glycogen synthase kinase-3β (GSK-3β) (Ser9) proteins were significantly reduced in MCF-7 cells, while there was no significant change in the expression of total Akt protein. However, after treatment with 1 μmol/L of deguelin for 6 hours, there was no apparent change in the expression of these 5 proteins. Conclusion: Deguelin can inhibit the phosphorylation of GSK-3β (Ser9) via inhibition of the phosphorylation of PTEN (Ser380) and PDK1 (Ser241) pathway, thus inducing apoptosis and inhibiting proliferation of MCF-7 cells.

AIM:To detect the changes of cystathionine β-synthase (CBS) expression in the brain following ischemia-reperfusion of hind limbs in the rats and to elucidate their significance .METHODS:Hind limb ischemia was in-duced by clamping infrarenal aorta with a microvascular clip and brain injury was made by following reperfusion .The brain tissue was obtained from the animals subjected to sham operation , 4 h of ischemia without reperfusion and 3 h, 6 h, 12 h, 24 h of reperfusion following 4 h of ischemia .The expression of CBS at mRNA and protein levels was measured at different time points by reverse transcription-polymerase chain reaction ( RT-PCR) and Western blotting .The CBS activity and hy-drogen sulfide ( H2 S) concentration in the brain were determined by a universal microplate reader .The observation of path-ologic changes of the brain was made following the inhibition of CBS by hydroxylamine .RESULTS:The relative expression of CBS at mRNA and protein levels in IR group significantly increased compared with sham group .It reached a peak at 12 h (P<0.01), and returned to baseline at 24 h (P>0.05).This time course correlated with increased CBS activity and H2 S concentration .No statistically significant difference in the above indexes between sham operation group and ischemia group was observed (P>0.05).Inhibition of CBS activity induced more severe brain injury in IR group .CONCLUSION:Up-regulation of CBS/H2 S pathway is involved in the protection for neurons during the ischemia-reperfusion of hind limbs .

Objective:Investigate the relation between the phosphorylation of FOXO1 and the apoptosis and the proliferation of lymphoma cells and to clarify its specific mechanism.Methods:The lymphoma cells Namalwa and Jurkat were treated with PI3K inhibitor wort mannin or etoposide or Wortmannin plus etoposide for different times-pan and at different concentration.The inhibition rates for cell growth of lymphoma cells were examined by XTT assay.Apoptosis were detected by flow cytometry.The expressions of p-Akt,p-FOXO1,FOXO1 and Bim were determined by Western blot analysis.Results:Wortmannin induced apoptosis of Jurkat cells and Namalwa cells and inhibited their survival effectively.The growth inhibition rate and the apoptosis rate of lymphoma cells induced by Wortmannin plus etoposide were higher than those induced by etoposide alone.After treated with Wortmannin,phosphorylation of FOXO1 remarkably reduced and bim markedly increased.Conclusion:The dephosphorylation of FOXO1 inhibits proliferation of Jurkat cells and Namalwa cells,promotes their apoptosis and enhanced the sensitivity of Non-Hodgkin lymphoma cells to etoposide.Bim activated by FOXO1 promotes cell apoptosis.