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 application of ultrasound-guided femoral nerve block (FNB) and lateral femoral cutaneous nerve block (LFCNB) for patients undergoing hip fracture surgery.Methods 60 patients scheduled for hip fracture surgery undergoing LMA general anesthesia were randomly divided into 3 groups,20 cases in each group.Before transfer patients from bed to operating table,A group received dezocine 5mg iv,B group received fascia iliaca compartment block(FICB),C group received FNB combined with LFCNB.40mL of 0.375％ ropivacaine was injected guiding by ultrasound in B group and C group.The time of sufficient sensory block and awake,the dosage of propofol and remifentanil,MAP and HR at pre-block (T1),20min after block (T2),transfer bed (T3),LMA insert (T4),skin incision(T5),LMA remove(T6) and sober(T7) were recorded.Pain was assessed using visual analogue scale(VAS) pre-and post block.The incidence of using vasoactive drugs,agitation,pain and adverse reaction were also recorded.Results The time of sufficient sensory block and awake,the dosage of propofol and remifentanil in A,B and C groups were as following:A group (not measured),(20.3 ± 1.3) min,(835 ± 6.7) mg,(1 285 ± 18) μg;B group (i2.2 ±2.7)min,(13.3 ± 1.4)min,(610 ±9.9)mg,(835 ± 15) μg;C group (9.7 ± 2.4)min,(12.8 ± 1.5) min,(555 ± 6.5) mg,(785 ± 16) μg.The time of awake,the dosage of propofol and remifentanil in B group and C group were significantly lower than those in A group(F =2.62,2.41,2.45,all P ＜ 0.05).The time of sufficient sensory block in C group was lower than that in B group (p ＜ 0.05).The MAP and HR at T2,T3,T5 and T7 in A,B and C groups were:A group (115 ± 4) mmHg,(90 ± 8) beats/min,(135 ± 6) mmHg,(98 ± 8) beats/min,(104 ±6) mmHg,(87 ± 4) beats/min,(120 ± 5) mmHg,(88 ± 8) beats/min;B group (102 ± 3) mmHg,(81 ± 6) beats/min,(112 ± 5)mmHg,(82 ± 8)beats/min,(89 ±6) mmHg,(72 ± 3) beats/min,(100 ±6)mmHg,(76 ± 8) beats/min;Cgroup (100 ± 3) mmHg,(80 x 6) beats/min,(109 ± 6) mmHg,(83 ± 5) beats/min,(86 ± 5) mmHg,(70 ± 3) beats/min,(99 ± 5) mmHg,(75 ± 5) beats/min.The levels of MAP and HR in B group and C group were significantly lower thanthose in A group(F =2.25,2.85,2.87,2.91,all P ＜ 0.05).The VAS scores at T2,T3,and T7in A,B and C groupswere:A group (3.9 ± 0.7) points,(8.2 ± 0.3) points,(6.0 ± 0.8) points;B group (2.3 ± 0.4) points,(4.1 ±0.4) points,(2.2 ± 0.7) points;C group (2.1 ± 0.5) points,(2.4 ± 0.4) points,(1.2 ± 0.4) points.The VAS scoresin B group and C group were significantly lower than those in A group (2.36,2.82,2.88,all P ＜ 0.05).The VASscores at transfer bed and sober in C group were significantly lower than those in B group (F =2.32,2.38,all P ＜0.05).The incidence of using ephedrine/atropine,urapidil/esmolol,PONV,agitation,pain and incision pain in A,Band C groups were:A group 30％,30％,25％,25％,40％;B group 10％,10％,0％,0％,10％;C group 10％,5％,0％,0％,0％.The number of patients who required vasoactive drugs and adverse reaction in B group and C group were significantly lower than those in A group(x2 =7.58,8.81,9.11,9.11,8.89,all P ＜0.05).The incidence of incision pain at sober in C group was lower than that in B group(x2 =9.21,P ＜ 0.05).Conclusion The ultrasound -guided FNB and LFCNB can obviously shorten the onset time,reduce the dosage of general anaesthetic and maintain the stability of henodynamics during the perioperative period.It has effective analgesia during transfer of patients from bed to operating table and sober.

AIM: To explore the effects of cellular signal transduction pathways of heme oxygenase-1(HO-1)-carbon monoxide (CO)-cyclic GMP (cGMP) and nitric oxide synthase (NOS)-nitric oxide (NO)-cGMP on cholecystokinin octapeptide (CCK-8) reversed vascular hyporeactivity in endotoxemic rats. METHODS: According to the treatments given in vivo , rats were devided into four groups: control; lipopolysaccharide (LPS); CCK and CCK+LPS. Using isolated vascular ring tension detecting technique, thoracic aortic rings (TARs) were prepared and accumulation of contractive responses to phenylephrine (PE) were measured under which the TARs were incubated with Hemin (He, donor of CO), Zinc-protoporphyrin-IX (ZnPP-IX, selective inhibitor of HO-1), L-arginine (L-Arg, substrate of NOS), aminoguanidine (AG, selective inhibitor of iNOS), N ?-nitro-L-arginine (L-NNA, inhibitor of NOS) or methylene blue (MB, inhibitor of guanylyl cyclase), respectively. RESULTS: CCK-8 alone did not affect vascular tension. Injection of LPS induced the hyporeactivity of the TARs and was reversed by pretreatment of CCK-8. In LPS and CCK+LPS groups, the hyporeactivity was partly reversed by incubation of TARs with ZnPP-IX or AG, and restored to normal by incubation of TARs with L-NNA or MB. Incubation of TARs with He or L-Arg showed to make the vascular hyporeactivity worse in different degree. CONCLUSIONS: CCK-8 alone did not affect the activity of HO-1 and iNOS but influenced the activity of these enzymes induced by LPS, which lead to reduced CO/NO production, decreased the content of cGMP and plays its important role in reversing vascular hyporeactivity in endotoxemic rats.

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.

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.

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.

Objective To investigate injecting recombinant human granulocyte-colony stimulating factor(rhG-CSF) on the proportion of peripheral neutrophilic granulocyte and their surface molecules expression in healthy people.Methods The peripheral blood samples were collected from the healthy people who were injected with rhG-CSF.The expressions of CD62L,CD11a,CD44 and CD49d on the surface neutrophilic granulocytes were determined before and after injection with flow cytometery.Results The median percentage of neutrophilic granulocytes in peripheral blood leucocytes after injecting rhG-CSF significantly increased from 60% to 85%(P0.10).Conclusion Injecting rhG-CSF may obviously impact the expression of CD62L and CD49d on neutrophilic granulocytes.