The clinical value of applying portal vein resection and reconstruction in left trisectionectomy for treating advanced hilar cholangiocarcinoma is approved, while it is still a big challenge for clinicians. One female patient suffering from abdominal pain and jaundice received treatment in the General Hospital of PLA in July, 2009. She was prelimiarily diagnosed with Bismuth type Ⅲ a hilar cholangiocarcinoma. A tube was inserted in the left lateral inferior bile duct to carry out percutaneous transhepatic biliary drainage (PTBD). After the anatomic variation of the left bile duct was found, the diagnosis was revised as Bismuth type Ⅳ. A left trisectionectomy was proposed, and another PTBD tube was inserted in the right posterior bile duct.Combined portal vein resection and reconstruction and left trisectionectomy was successfully performed. The postoperation course was uneventful, except for the transient liver dysfunction and biliary-enteric anastomotic leakage.

Four-week-old male Sprague-Dawley rats were rendered diabetic by intraperitoneal injection of streptozotocin (STZ) after feeding high-fat-diet for 8 weeks,and divided into diabetes group and tumor necrosis factorrelated apoptosis ligand(TRAIL) group.Normal rats severed as a control group.Treatment with TRAIL lasted for 3 months.Total cholesterol,triglycerides,low-density lipoprotein-cholesterol,blood glucose,and insulin levels were decreased in TRAIL group,as compared with diabetes group.Area of atherosclerotic lesion in TRAIL group [(23.8 ± 5.7) ％] was significantly smaller than that in diabetes group [(47.6 ± 7.8) ％].It suggested that TRAIL may reduce the area of atherosclerotic lesion in diabetic rats.

Objective To explore the effect and its mechism of osteoprotegerin (OPG) on human umbilical vein endothelial cells(HUVECs) induced by high glucose.Methods (1) The cultured HUVECs were treated with normal glucose(5.5 mmol/L),high glucose(33 mmol/L),high glucose + OPG(0.5,1,and 2 μg/ml)as well as mannitol(5.5 mmol/L glucose+27.5 mmol/L mannitol) for 48 h,respectively.Flow cytometry assay and Hoechst 33258 staining were used to detect the cell apoptosis.The expression levels of Bcl-2 and Bax protein were measured by western blot analysis.(2) The cultured HUVECs were treated with normal glucose,high glucose,high glucose + OPG (2 μg/ml OPG),high glucose + rapamycin(10 ng/ml rapamycin) as well as high glucose + rapamycin + OPG for 24h,respectively.The expression levels of S6K,p-S6K,4EBP1 and p-4EBP1 protein were measured by western blot analysis.(3)The cultured HUVECs were treated with normal glucose,high glucose,high glucose + OPG(2 μg/ml)for 24 h,respectively.The expression levels of tuberin and p-tuberin protein were measured by western blot analysis.Results (1) Compared with normal glucose group,the apoptosis of HUVECs and the expression level of Bax was dramatically increased,and the expression of Bcl-2 was decreased significantly in high glucose group (P＜0.05).The apoptosis of HUVECs and the expression level of Bax in high glucose + OPG group was significantly lower than that in high glucose group,which was still higher than that in normal glucose group (P＜ 0.05).and the expression of Bcl-2 in high glucose + OPG group was significantly higher than that in high glucose group,which was still lower than that in normal glucose group (P＜0.05).There was no statistically difference between hyperosmolar control group and normal glucose group.(2) Compared with normal glucose group,the expression levels of p-S6K and p-4EBP1 were increased markedly in high glucose group(P＜0.05).The expression levels of p-S6K and p-4EBP1 in high glucose + OPG group were significantly lower than that in high glucose group,which were still higher than that in normal glucose group(P＜0.05).No significant difference was found between high glucose + OPG group and high glucose + rapamycin group.(3) Compared with normal glucose group,the expression level of p-tuberin was increased markedly in high glucose group (P ＜ 0.05).The expression level of p-tuberin in high glucose + OPG group was significantly lower than that in high glucose group,which was still higher than that in normal glucose group (P ＜0.05).Conclusions It suggests that the protective effect and mechanism of OPG on HUVECs cultured with high glucose may be association with tuberin/mTORC1 pathway.

Objective To investigate the protective effect and mechanisms of NF-?B decoy oli- godeoxynucleotides(ODNs)on rat liver graft following ischemia-reperfusion injury.Methods Ani- mals were randomly divided into 3 groups(n=8 in each group):control group,ischemia-reperfusion (IR)group,and decoy ODNs group,in which donor grafts were transfected with 120?g NF-?B decoy ODNs before graft procurement.Following 2 h of reperfusion,Kupffer cells(KCs)were isolated,and NF-?B biding activity was detected with electrophoretic mobility shift assay(EMSA),and TNF-?、IL- 6 mRNA expression was assayed by using RT-PCR method.Meanwhile,the liver and serum samples were collected,the histopathologic change of liver was examined by light microscope,and liver func- tion was analyzed.Results The NF-?B biding activity,TNF-?,IL-6 mRNA expression,and the ALT,TBIL levels in serum were significantly increased following 2 h of reperfusion in IR group as compared with those in control group(P＜0.01).A large amount of degeneration and necrosis in hep- atocytes accompanied with obvious congestion in hepatic sinusoid occurred.However,these tested in- dexes were significantly ameliorated in decoy ODNs group as compared with those in IR group(P＜0.01),and the architecture of hepatic lobules was remained.Conclusions KCs NF-?B activation fol- lowing reperfusion plays an important role in IRI in liver transplantation.Decoy strategy shows appar- ent effect on suppression of NF-?B activation,and thus inhibits the production of downstream cyto- kines,which protects the liver graft from IRI.

Probability of causation (PC) was used to facilitate the adjudication of compensation claims for cancers diagnosed following exposure to ionizing radiation. In this article, the excess cancer risk assessment models used for PC calculation are reviewed. Cancer risk transfer models between different populations, dependence of cancer risk on dose and dose rate, modification by epidemiological risk factors and application of PC are also discussed in brief.

Objective To investigate the effect of growth differentiation factor 11 ( GDF11 ) on aorta in apolipoprotein E-Null( ApoE-/-) mice and its possible mechanisms. Methods Four-week-old healthy male ApoE-/-mice were fed with high-fat diet for 1 week and were then divided into 4 groups:vehicle group(n=10), GDF11 group (n=10),adeno-associated virus-green fluorescent protein group(AAV-GFP group, n=10), and AAV-GDF11 group ( n=10 ) . The mice received intraperitoneal injection with phosphate buffered saline, GDF11 protein, a single injection of purified AAV-GDF11 or AAV-GFP through the tail vein, respectively. After 4 weeks, serum GDF11/8 level and endothelium-dependent vasodilatation were detected. After 12 weeks, serum GDF11/8, interleukin-6 (IL-6), tumor necrosis factor-α( TNF-α), total cholesterol ( TC), triglycerides ( TG), oxidized low density lipoprotein(ox-LDL), and free fatty acids(FFA)levels were measured, the plaque areas in aortic enface and cross sections were measured by oil red O or HE staining, the macrophages/T lymphocytes infiltration in plaques were detected with immunohistochemistry, and the mRNA expressions of IL-6, TNF-α, and IL-10 were determined by real-time PCR. Results Compared with vehicle or AAV-GFP groups, GDF11 and AAV-GDF11 groups presented improved endothelium-dependent vasodilatation, decreased levels of blood inflammatory factors, blood lipid, reduced plaque on face area sections[Vehicle group : GDF11 group:(31. 23 ± 3. 12)% vs (17. 18 ± 2. 17) %;AAV-GFP group : AAV-GDF11 group:(38.01±4.43)% vs(14.54±2.86)%,P<0.05]andcrosssections[Vehiclegroup :GDF11 group:(19. 87 ± 2. 11)% vs (10. 32 ± 1. 47)%;AAV-GFP group : AAV-GDF11 group:(23. 02 ± 2. 76)%vs (9.06±1.63)%, P<0. 05]. There were less macrophages and T lymphocytes infiltration in plaques and lower mRNA expressions of inflammatory factors at aortic wall. Conclusion GDF11 reduces the area of atherosclerotic lesion in ApoE-/-mice, which may be involved in endothelial protection, such as to reduce inflammatory reaction, and to change cellular composition in plaques.

Objective: To explore the effect of irisin on atherosclerosis with possible mechanisms in diabetes mellitus (DM) mice. Methods: A total of 30 ApoE-/- mice were randomly divided into 2 groups: Control group, the mice received citrate buffer solution for modeling control,n=10. DM group, the mice received streptozotocin injection for DM modeling,n=20; the DM group was further divided into 2 subgroups as DM control (DM-C) group, the mice received normal saline injection for 12 weeks and DM + irisin group, the diabetic mice received irisin injection for 12 weeks.n=10 in each subgroup. With 4 weeks of irisin intervention, the endothelium-dependent vasodilatation was detected. With 12 weeks of intervention, the blood levels of tumor necrosis factor-α (TNF-α), high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6) and oxidized low-density lipoprotein (ox-LDL) were examined by ELISA, the plaque areas in aortic en face and cross sections were measured by Oil red O or HE staining, the macrophages/T lymphocytes inifltration in plaques were detected with immunohistochemistry, and the mRNA expressions of IL-6, IL-10, TNF-α were determined by RT-PCR. Results: Compared with DM-C group, DM + irisin group presented improved endothelium-dependent vasodilatation, decreased levels of blood inlfammatory factors, reduced plaque on face area sections (22.57 ± 2.17) % vs (35.09 ± 2.38) % and cross sections (19.36 ± 1.85) % vs (25.53 ± 7.87) %,P < 0.05, less macrophages (30.5 ± 2.79) % vs (41.34 ± 9.13) % T and lymphocytes infiltration (28.11 ± 4.24) % vs (35.79 ± 9.11) % in plaques and lower mRNA expressions of inflammatory factors(IL-6: 1.76 ± 0.50 vs 3.78 ± 1.15; TNF-α: 1.05 ± 0.30 vs 2.11 ± 0.48; ICAM-1: 1.96 ± 0.69 vs 2.71 ± 0.72; VCAM-1: 0.87 ± 0.21vs 1.45±0.25; MCP-1: 1.34 ± 0.34 vs 1.77 ± 0.55) at aortic wall, P<0.05.Conclusion: Irisin may improve atherosclerosis condition in ApoE-/- DM mice, the endothelial protection and antiinflammatoryreaction were the important mechanisms. Irisin has the potential for preventing/treating atherosclerosis.

Objective To investigate the effects of growth differentiation factor 11 ( GDF11 ) on β-cell function in db/db mice and its possible mechanism. Methods Twenty eight-week-old male db/db mice were randomizedtoi.p. administration of GDF11(0.3mg·kg-1·day-1)or equivalent PBS(n=10)for 6 weeks.10age-matched male db/m were used as normal control, received equivalent PBS injection for 6 weeks. Blood glucose levels, body weights and food intake were monitored weekly. IPGTT and glucose-stimulated insulin secretion ( GSIS) were analyzed. After 6 weeks of intervention, serum HbA1C , TG, TC, and FFA were measured respectively. The concentrations of hormones in serum and pancreas were evaluated. The mRNA expression of Pdx-1, MafA, Nkx6. 1, and insulin2 were determined by RT-PCR. The expression of phosphorylated Smd2 (P-Smad2), Smad2 in islet were examined by western blot. Results Compared with NC group, GDF11 administration decreased FBG, HbA1C , modified lipid profiles. GDF11 improved glucose tolerance and augmented GSIS. Moreover, GDF11 increased serum insulin and pancreatic insulin content, while decreased serum glucagon concentration. The expression of Pdx-1, MafA, Nkx6. 1, and Insulin2 were significantly increased in GDF11 group. GDF11 elevated the expression of P-Smad2 in islets. Conclusion s GDF11 may preserve β-cell function and facilitate the secretion and production of insulin. Diminishing the metabolic abnormalities, alleviating the secretion of glucagon, as well as maintaining the key transcript factor activation may contribute to the amelioration of β-cell function after GDF11 administration. Smad2 pathway may be related to the protective effects of GDF11.

AIM: To investigate the effect of problem - based learning ( PBL) used in the teaching of medical students'evidence-based medicine ( EBM) .
METHODS: Five classes ( total 147 students ) were randomly selected as experimental ( PBL ) group, at the same time, another 5 classes ( total 149 students ) were also randomly selected as control group, using traditional teaching method ( lecture-based learning, LBL ) in 2010 grade. The final examination scores of the experimental group were compared with control at the end of term. In addition, all students were interviewed using self -administered questionnaire to obtain their evaluation for PBL practice. SPSS13. 0 software was used for statistical analysis.
RESULTS: The homogeneity test in baseline survey showed that the basic characteristics between the two groups of students were no significant differences, and were comparable (P>0. 05). Final exam results showed that in addition to the scores of the EBM basic knowledge indicated no significant difference between two groups of students (P>0. 05), for the 5 steps of EBM procedure, namely, asking questions, finding the best evidence, evaluating the evidence, using and practicing the evidence, re - evaluating the evidence, and the total scores between the two groups, there were significant statistically differences (P<0. 05). The results to student learning evaluation showed that there was no significant difference between the two groups (P>0. 05) in aspects of better understanding classroom knowledge, improving language expression ability, and writing skill exercises. And other residual items had a significant difference ( P<0. 05), especially in aspects of improving enthusiasm for learning, self - study ability, improving learning efficiency, information analysis and utilization ability, team collaboration, and communication between teachers and students, however, there was a very significant difference (P<0. 001) between the two groups.
CONCLUSION: PBL teaching mode can effectively improve teaching effectiveness and the quality of EBM teaching, so the this teaching mode is worth further popularizing.

Objective To study the effect and mechanisms of berberine (BBR) on the proliferation of papillary thyroid cancer K1 cells induced by high glucose.Methods K1 cells were cultured under 5.5 mmol/L or 25 mmol/L glucose condition with or without different concentration of BBR (0,10,40 and 80 μmol/L) for 24 hours.The proliferations of K1 cells in each condition were detected by MTT.Western blot was used to measure the expression of nuclear factor erythroid 2-related factor 2 (Nrt2),phosphoinositide 3-kinase (PI3K),protein kinase B (Akt) and phosphorylated-Akt (p-Akt).The distribution pattern of Nrf2 in K1 cells was determined using immunofluorescent staining.Results Compared with 5.5 mmol/L condition,the proliferation rate [(126.64 ± 5.41) ％ vs (87.31 ± 3.67) ％],expression levels of PI3K (0.425 ±0.019 vs 0.272 ±0.039),p-Akt/Akt (0.446 ±0.021 vs 0.168 ±0.035) and Nrf2 (0.597 ± 0.014 vs 0.308 ± 0.026),and Nrf2 distribution (93.0％ vs 23.1％) in nuclear of K 1 cells under 25 mmol/L condition were significantly elevated,respectively (all P ＜0.01).Addition of BBR in 25 mmol/L condition dose dependently (10,40,80 μmol/L) lowered the proliferation rate of K1 cells [(111.76 ± 4.10)％,(70.03 ±2.18)％,(32.41 ±3.76)％ vs (126.64 ±5.41)％,all P＜0.05],and suppressed the expression of PI3K,p-Akt/Akt,Nrf2,and Nrf2 nuclear distribution (P ＜ 0.05).Conclusions BBR dose dependently inhibited the proliferation of high glucose-induced K1 cells.This effect was associated with the suppression on of PI3K/Akt signaling activation,Nrf2 expression and its nuclear translocation.