Objective:To investigate the mechanism of CTIL-4Ig combined with Anti-ICAM-1 mAb in promoting immune tolerance induced by donor-derived immature dendritic cells(imDC) in recipient mice.Methods: Male mice were divided into 4 groups: control group(receiving only imDC),CTLA-4Ig group,ICAM-1 mAb group and CTLA-4Ig+ICAM-1 group.Mice were transfused with donor-derived imDC 7 days before they received heart transplantation in company with daily injection of ICAM-1 mAb,CTLA-4Ig or both for the following 2 weeks.Immunological analysis was performed in mice 7 days and 21 days after heart transplantation.Results: CTLA-4Ig alone or in combination with ICAM-1 mAb significantly inhibited T cells proliferation to alloantigen stimulation,impaired lymphocyte cytotoxicity,suppressed production of IL-2,IFN-? by Th1,increased production of IL-10,and obviously decreased the production of alloantibody IgG in recipient mice treated with donor-derived imDC.ICAM-1 mAb alone had no significant effects on T cells proliferation and production of Th-derived cytokines except for IL-2.Conclusion: ICAM-1 mAb combined with CTLA-4Ig can enhance immune tolerance induced by donor-derived imDC in recipient mice through induction of T cells hypo-responsiveness,inhibition of lymphocyte cytotoxicity and B cell immunoreation,and promotion of Th2 polarization in vivo.

Liver transplantation has been taken as one of the most effective therapies for patients with end-stage liver disease. However. 10%-40% patients develop biliary complications (BO after transplantation and 6%-13% patients have to receive liver retransplantation, with the mortality being around 19%. BC is one of the major risk factors for the prognosis of liver transplantation. This review summarizes the etiology and the mechanism(s) of biliary complications after liver transplantation.

Objective To summarize the experience of liver retransplantation, as well as the factors i nfluencing the surgical effects. Methods The clinical data of 8 patients who received liver retransplantation in our cent er were analyzed retrospectively. Results Among 8 cases, complications of biliary tract occurred in 5 cases, chronic rejec tions in 2 cases, embolism in hepatic artery in one case. Infections occurred in 7 cases before engraftment. Case 1 had develope d renal function failure before the surgery, and he died of severe infections an d multi-organ failure after transplantation. Case 4 had massive hemorrhage duri ng the operation and also died of multi-organ failure after transplantation. Case 7 developed in tracanial hemorrhage and abdominal infection and died early after transplantatio n. Other 5 cases has recovered and left hospital. Conclusions Liver retransplantation is the only measure that can be taken to save the lives of patients whose liver allograft fails to function. It's very important that the indications and time of retransplantation should be carefully selected. Factors that may lead to harmful effects on liver retranspl antation include bad preoperative condition of the recipient, tough and long ope ration, massive hemorrhage during the operation, and severe complications after the surgery.

The understanding of anatomical structures and their adjacent relationship is the founda-tion and key to the development of surgical skills and clinical thinking. In clinical teaching for residents and graduate students , we took the advantage of donor operations in organ transplantation and showed abdominal anal operations anatomical features and relationships through different view angles and compre-hensive ways. This new teaching approach was designed in accordance with processes of organ donation, procurement and back-table operation. The main contents included anatomy of abdominal wall layers, rela-tionships among abdominal organs, locations and courses of important structure, as well as medical human-istic education. In the context of organ donation becoming more and more popular and standardized after the cardiac death of Chinese citizens, this teaching approach is worth exploring.

AIM:To observe the dynamic changes of neurokinin A(NKA) and calcitonin gene-related peptide(CGRP) levels in gastric mucosal and plasma in rats after abdominal seawater-immersing trauma,and to investigate the influence of these two sensory neuropeptides on acute gastric mucosal lesion.METHODS:Thirty-two SD rats were randomly divided into four groups(normal group,celiac seawater-immersing trauma 1,2 and 3 h groups).With emzyoimmunoassay and radioimmunoassay respectively,gastric mucosal and plasma NKA and CGRP levels in rats were measured.RESULTS:Compared with normal rats,with the seawater-immersing time prolonged,gastric mucosal NKA and CGRP levels in rats were progressively decreased(P

To explore the effects of astilbin on the maturation and immunologic function of mouse bone marrow-derived dendritic cells (DCs).

Objective To investigate the protective effect of a COX inhibitor,flurbiprofen (Flurb) on hepatic ischemia/reperfusion (IR) injury in rats and the action mechanism.Method C57BL/6 mice were randomized into sham,IR and Flurb (4 different doses) groups.The model of segmental (70％) warm hepatic ischemia was established in IR and Flurb groups.Flurbiprofen of different doses (5,7.5,10 and 15 mg/kg) was injected via the tail vein 20 min before ischemia.At different time points after reperfusion,liver cell necrosis and apoptosis were evaluated by HE and TUNEL staining.The COX and inflammatory cytokine gene expression was detected by using realtime PCR.Liver mitochondria were separated and mitochondrial permeability transition (MPT) pore sensitivity was examined by using swelling assay and fluorescence spectrophotometry assay.Result In flurbiprofen groups of different doses,the serum AST and ALT levels were significantly decreased at 6 h after reperfusion as compared with IR group.Moreover,10 mg/kg Flurb pretreatment significantly inhibited the mitochondrial permeability transition (MPT) pore opening,and thus alleviated liver cell damage and prevented mitochondria-related cell death and apoptosis by inhibiting COX-2 and inflammatory factor genes expression such as IL-1β,IL-6 and TNF-α.Conclusion Flurbiprofen protects mice from hepatic I/R injury possibly by inhibiting mitochondrial permeability transition and IL-1β,IL-6 and TNF-α expression,which may provide experimental evidence for clinical use of flurbiprofen to protect liver function in surgical settings other than its conventional use for pain relief.

Objective To study the effect of serf-designed multi-organ preservation solution(SMO)on cold-stored rat liver.Methods The rat livers were preserved with SMO solution(group A,n=15),UW solution(group B,n=15)and HC-A solution(group C,n=15),respectively.The livers were transplanted orthotopically after 6-,12-,24-hour preservation.The changes of liver function at hour 12 after transplantation were detected and conditions of the survived rats at day 14 after transplantation were observed.Results There was no morphological change of the livers in group A within 24 houm.The total bilimbin,alaninetransaminase,and hyaluronic acid increased in group A and B as the preservation time increased,but the levels of the 3 indexes of group A were significant lower than those in group C(F=49.027,70.280,34.349,71.532,446.544,303.408,P＜0.05).No rat djed in group A 14 days after liver transplantation.Conclusions SMO and UW solution have similar effect on protecting the liver.and the protective effect of the 2 solutioas was better than that of HC-A solution.

Objective To study the effects of Sinomenine on the dendritic cells after hepatic ischemia-reperfusion. Methods Forty-eight BN rats were equally divided into control group, low dose (40 μg/g) and high dose (80 μg/g) of Sinomenine groups after the liver transplantation models were established by two cuff tech-nique. Three days after the orthotopic liver transplantation, the livers were resected, then the dendritic cells were separated and purified. The phenotypes [OX62, major histocompatibility complex Ⅱ (MHC-Ⅱ) and CD86] of dendritic cells were examined by FACS, the expression of IL-12, IL-1, and TNF-a mRNA by RT-PCR, and the expression of Toll-like receptor 4 (TLR4) by Western blot. Results The dendritic cells treated with Sinomenine showed immature phenotypes. The expressions of MHC-Ⅱ and CD86 were significantly deceased. The expressions of IL-12, IL-1, TNF-a mRNA and TLR4 were low. Conclusions Sinomenine can significantly inhibit the maturity and immunologic function of dendritic cells after hepatic ischemia-reperfusion.

Objective To evaluate the protective effect of hydrogen-rich saline on renal ischemia/reperfusion (I/R) in mice. Methods Thirty C57BL/6 mice were randomly divided into 3 groups: sham-operated (SO) group, I/R group (mice were injected with 5 ml/kg saline by tail vein just before ischemia induction) and hydrogen-rich saline group (mice were injected with 5 ml/kg hydrogen-rich saline). At the 6th h after reperfusion, the sera and renal samples subject to IR injury were collected. The Scr and BUN levels in serum were determined and renal histological changes were also examined. The apoptosis of renal tubular epithelial cells was measured by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling assay. Malondialdehyde (MDA) contents in renal samples were measured using specific kits. The infiltration of F4/80 positive macrophages and neutrophils was assayed by using immunohistochemistry. The mRNA expression of TNF-α, IL-6, IL-1β and IL-17 was detected by using real time reverse transcription PCR. Results As compared with LR group, at the 6th h following reperfusion the levels of Scr and BUN were significantly reduced (P<0.05), histological changes obviously alleviated (P<0.01), apoptosis of renal tubular epithelial cells and MDA contents was decreased (P<0.05) in hydrogen-rich saline group. Moreover, the infiltration of macrophages and neutrophils, and the mRNA expression of TNF-α, IL-6, IL-1β and IL-17 in renal tissue in hydrogen-rich saline group were also declined as compared with IR group (P<0.05). Conclusion Hydrogen-rich saline can ameliorate renal IR injury to some extent, which is associated with inhibition of inflammatory response induced by reperfusion.