Establishment of a sensitized canine model for kidney transplantation

Objective:To establish a sensitized canine model for kidney transplantation. Methods: 12 male dogs were averagely grouped as donors and recipients. A small number of donor canine lymphocytes was infused into different anatomic locations of a paired canine recipient for each time and which was repeated weekly. Specific immune sensitization was monitored by means of Complement Dependent Cytotoxicity (CDC) and Mixed Lymphocyte Culture (MLC) test. When CDC test conversed to be positive and MLC test showed a significant proliferation of reactive lymphocytes of canine recipients, the right kidneys of the paired dogs were excised and transplanted to each other concurrently. Injury of renal allograft function was scheduled determined by ECT dynamic kidney photography and pathologic investigation. Results:CDC test usually conversed to be positive and reactive lymphocytes of canine recipients were also observed to be proliferated significantly in MLC test after 3 to 4 times of canine donor lymphocyte infusions. Renal allograft function deterioration occurred 4 d post-operatively in 4 of 6 canine recipients, in contrast to none in control dogs. Pathologic changes suggested antibody-mediated rejection (delayed) or acute rejection in 3 excised renal allograft of sensitized dogs. Seven days after operation, all sensitized dogs had lost graft function, pathologic changes of which showed that the renal allografts were seriously rejected. 2 of 3 dogs in control group were also acutely rejected. Conclusion：A convenient method by means of repeated stimulation of canine lymphocyte may induce specific immune sensitization in canine recipients. Renal allografts in sensitized dogs will be earlier rejected and result in a more deteriorated graft function.     

Expression of cytokines in mouse hepatitis B virus X gene-transfected model

The expression profile in the mouse hepatitis B virus X (HBx)-transfected model was investigated in order to lay a foundation for further study on the implication of cytokines expression in hepatitis B virus (HBV) infection.Hydrodynamic injection method via the tail vein was used to establish the animal HBx-transfected model.By using microassay,the differential expression of gene in each group was analyzed,which was further confirmed by using real-time PCR and semi-quantitative PCR.Most of chemokine genes such as Ccl2,Ccl5,Ccl9,MIG and IP-10 were up-regulated in the HBx-transfected mouse model versus the control mice,which was coincided with the microarray results.Western blotting and immunohistochemistry were applied to detect the expression of MIG and IP-10 in the liver tissues.Simultaneously,ELISA was adopted to measure the content of IFN-γ in the liver tissues.DNA microassay revealed that the expression of 611 genes changed in HBx-transfected mice as compared with that in pCMV-tag2B-transfected mice,and most of the screened chemokines were up-regulated (including MIG and IP-10).Additionally,IFN-γ protein levels were increased by 20.7% (P<0.05) in pCMV-tag2B-HBx-transfected mice as compared with the untreated mice.IFN-γ protein levels were reduced by 53.9% (P<0.05) in pCMV-tag2B-transfected mice as compared with the untreated mice,which was consistent with the up-regulation of MIG and IP-10.It was suggested HBx transfection could induce the expression of MIG and IP-10 in the liver tissues,which might play the roles in HBV-related liver immunity and cytokines-mediated antiviral effect.     

Study on effect and mechanism of sodium ferulate in preventing and treating ozone induced lung injury in mice

Objective:To study the effect and mechanism of sodium ferulate (SF) in preventing and treating ozone (O_3) induced lung oxidative injury in mice.Methods:Lung oxidative injury model mice were established by making them inhale O_3.The activity of anti-oxidase and membranous microviscosity in epithelial cells in the lung of mice were determined,and the ultrastructural change of lung tissues was observed with electromicroscopy.Results:Activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were reduced,while membranous lipo-microviscosity significantly increased in the pulmonary epithelial cells of model mice,revealing ultrastructural change.These abnormal changes were reversed by SF treatment,which was manifested as the significantly raised activities of SOD and GSH-Px after treatment with high and moderate doses of SF,showing a significant difference compared with those in the model group (P<0.01).Membranous lipo-microviscosity basically approached that in the control group (P>0.05);electron microscopic examination showed a basically normal morphological structure of pulmonary epithelial cells,with the change in lung injury significantly milder than that in the model group.Conclusion:O_3 could induce oxidative injury of lungs in mice,and SF could enhance the anti-oxidation capacity of mice and scavenge the oxygen free radicals so as to alleviate the injury.     

Transgenic mice with overexpression of human scavenger receptor A on endothelial cells

Objectives To establish a new transgenic mouse model for determining the function and role of human scavenger receptor A (SR- A) in atherosclerosis in vivo. Methods Human scavenger receptor minigene- driven mouse tie- 1 promoter was constructed and confirmed by endonuclease digestion and sequence analysis. Transgenic mice were generated via the microinjection method. PCR and Southern blot were used t o screen the positive transgenic mice. RT- PCR and immunohistochemical analysis were used to detect the level and location of human SR- AⅠ expression in transgenic mice. The activity of human SR- AⅠ was determined by morphologi c observation of aortic endothelial cells of transgenic mice under transmission electron microscopy. Results The electrophoresis assay showed the expected 4 fragments of 0. 9 kb, 1. 1 kb, 1. 2 kb and 4. 2 kb in the SmaⅠ digest and 2 fragments of 0. 8 kb and 6 . 7 kb in BglⅡ digest of plasmids pTie- 1/hSR- A. The fragment sequence of tie - 1 p romoter and human SR- A cDNA in plasmids pTie- 1/hSR- A was correct and no A TG b efore the translation initiation sites of human SR- A was found by sequence ana lysis. 561 injected and surviving embryos with the purified human SR- A minigen e were implanted into the oviducts of 19 ICR pseudopregnant mice. Among the 54 surviving pups from 13 foster mothers, 7 were identified by PCR and Sou thern blot analysis. The results of RT- PCR and immunohistochemical analysis sh owed human SR- A was specifically expressed on vascular endothelial cells of the aorta and renal artery, as well as hepatic sinusoidal endothelial cells in tran sgenic mice. Transmmion electron microscope (TEM) of aorta of transgenic mice s howed that a large number of vesicles, multivesicle bodies and swollen mitochond ria filled the plasma of endothelial cells. Conclusions A transgenic mouse model with overexpression of human SR- A in endothelial cells was successfully established. The transgene was integrated and transmitted int o the chromosome of transgenic mice. Tie- 1 promoter controlled the transgene t o express in endothelial cells in mice. Pinocytic activity of aortic endothelia l cells in transgenic mice was higher than that of C57BL/6J mice. Our studies w ill provide a new transgenic model for investigation of atherosclerosis and func tions of human SR- A.     

Hybrid Endovascular Aorta Repair with Simultaneous Supra-aortic Branch or Iliac Branch Revascularization

Objective To describe a hybrid endovascular procedure for aorta repair with different kinds of bypass followed by concomitant placement of stent graft in the aorta. Methods From June 2007 to May 2008, 5 consecutive patients who presented with aortic aneurysm or dissection were treated with a new hybrid aorta repair technique. Complete surgical rerouting of supra-aortic vessels was simultaneously created by endovascular repair of aortic arch aneurysm with stent graft. Hybrid left carotid-subclavian bypass with stent graft deployment covering the ostium of the left subclavian artery was performed in a Debakey type III aortic dissection case. The supra-aortic branch was revascularized in 2 cases from ascending aorta to bilateral common carotid arteries using a 16-8 mm bifurcated graft, then total aortic arch and descending artery was occluded with stent-graft. The left carotid artery to the left subclavian artery bypass was created in 1 case, followed by stent-graft deployment. Two cases of infrarenal abdominal aortic aneurysm underwent left external iliac artery to left internal iliac artery bypass by a retroperineal route, then hybrid procedure was performed with bifurcated stent-graft. All stent grafts were deployed via a retrograde femoral artery approach in 5 patients. Results Technical success with complete aneurysmal exclusion was achieved in all patients. There was no incidence of encloleak. During a follow-up period of 2 to 10 months, documented perioperative neurologic events did not occur in all patients. One patient suffered from adult respiratory distress syndrome. After received tracheostomy, he recovered later. There was one death resulting from a postoperative myocar- dial infarction. Conclusion Hybrid arch repair provides an alternative therapy to patients otherwise considered prohibitively high risk for traditional open arch and thoracoabdominal aorta repair.     

A murine model of mixed bone marrow transplant:importance of the splenocytes to balance HVG and GVH reactions

Objective: A murine model of mixing syngeneic and haploidentical major histocompatibility complex (MHO matched bone marrow cells transplant was used to evaluate the effect of splenocytes in graft-versus-host disease (GVHD) and host-versus graft reaction (HVGR). Methods: BALB/C recipient mice were lethally conditioned with 8. 5 Gy and injected with different grafts which consisted of syngcneic bone marrow cells plus splenocytes (SPLCs) and haploidentical MHC matched hone marrow cells (BMCs) plus different closes of splenocytes. Recipient mice were detected for the percentage of haploidentical MHC matched mouse origin cells in the peripheral blood cells and checked daily for the appearance of GVHD symptoms. Histopathological examination of multiple organs from moribund mice was used to evaluate the grades of GVHD. Results: Recipient mice infused with 10×106 haploidentical MHC matched SPLCs and 5×106 syngeneic splenocytes showed a higher level and more stable chimerism with GVHD II degree histopathological alterations. Histopathological results of GVHD in other group's hosts were not obvious, and the levels of chimerism were unstable. All of the mice survived over 150 d. Conclusion:The proportion and dose of syngeneic and haploidentical MHC splenocytes are of importance for inducing stable en-graftment on the basis of nonlethal GVHD and to balance GVHD and HVGR.     

Expression of NADPH oxidase and production of reactive oxygen species in aorta in an active immunization mouse model with AT1-EC2 peptide

The antibody against AT1-EC2 plays a role in some kinds of inflammatory vascular diseases including malignant hypertension,preeclampsia,and renal-allograft rejection,but the detailed mechanisms remain unclear.In order to investigate the changes of NADPH oxidase and reactive oxygen species in the aorta in a mouse model which can produce AT1-EC2 antibody by active immunization with AT1-EC2 peptide,15 mice were divided into three groups:control group,AT1-EC2-immunized group,and AT1-EC2-immunized and valsartan-treated group.In AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group,the mice were immunized by 50 μg peptide subcutaneously at multiple points for 4 times:0,5,10,and 15 days after the experiment.In AT1-EC2-immunized and valsartan-treated group,valsartan was given at a dose of 100 mg/kg every day for 20 days.After the experiment,the mice were sacrificed under anesthesia and the aortas were obtained and frozen in liquid nitrogen for the preparation of frozen section slides and other experiments.The titer of AT1-EC2 was assayed by using ELISA.The level of NOX1 mRNA in the aorta was determined by using RT-PCR.The expression of NOX1 was detected by using Western blotting.Confocal scanning microscopy was used to assay the α-actin and NOX1 expression in the aortic tissue.The O 2.production was detected in situ after DHE staining.The mice produced high level antibody against AT1-EC2 in AT1-EC2-immunized group and AT1-EC2-immunized and valsartan-treated group,and the level of NOX1 mRNA in the aortic tissues was 1.6±0.4 times higher and the NOX1 protein expression was higher in AT1-EC2-immunized group than in control group.There were no significant differences in the level of NOX1 mRNA and protein expression between control group and AT1-EC2-immunized and valsartan-treated group.The expression and co-localization of α-actin and NOX1 in AT1-EC2-immunized group increased significantly as compared with those in control group,and the O 2.production increased about 2.7 times as compared with contro     

A SD rat model of thoracic aortic aneurysms

Backgroud Thoracic aortic aneurysm (TAA) disease is a serious condition with both high mortality and morbidity rates associated with surgical therapy. Further understanding of the formation and progression of TAAs may provide novel, less invasive therapeutic strategies in patients with this devastating disease. Aneurysm formation is a complicated, dynamic process involving both cellular and extracellular processes. The mechanisms of TAA formation are poorly understood, mainly due to the lack of a useful and reproducible model. In 2003, Ikonomidis in South Carolina developed a murine model of TAA.The mouse model was less satisfactory because the small size of the murine aorta. The rat model has the advantage of larger aorta and the ability to do more research. Proper animal models are useful to understand the aetiology and evolution and they can be used to evaluate the efficacy of new treatments.Objective The goal of this study was to test the hypothesis that abluminal calcium chloride application could creat TAAs in the SD rats.MethOds Eight-week-old male Sprague-Dawley(SD) rats(n=60) were divided into two groups equally. All rats were anesthetized. An angiocath was then advanced through the mouth into the trachea under direct vision and connected to a rodent ventilator set at a respiratory rate of 180 breaths per minute. And their thoracic aortas were exposed via left thoracotomy. In the experiment group,a sponge soaked in 0.5 mol/L CaCl2 was placed on the distal half of the exposed descending thoracic aorta under direct vision. As control group, 0.5 mol/L CaCl2 was instead of 0.9% NaCl. After 15 min, the sponge was removed. Then the chest was closed. At 4,8,12 weeks, all animals undergoing fixation and aortic harvest were reanesthetized and the thorax was then opened beneath the xiphoid process. Potassium chloride was injected into the left ventricle under direct vision to arrest the heart. Then it was perfusion program and the entire animal was immersed in formalin. Seven days after fixation, the animal was removed from formalin, and the aorta was carefully harvested from its root to the renal arteries. The aorta was then immersed in an individually labeled jar containing a mixture of 80% methanol and 20% dimethyl sulfoxide (Dent's solution).Diameter measurements were made using Axioplan 2 imaging system. Hematoxylin and eosin staining and Van Gieson and Verhoeff staining showed the elastic architecture and collagen structure. Immunohistochemical staining was performed to evaluate the presence of lymphocytes and macrophages. Results 12 weeks of CaCl2 treatment resulted in visually obvious dilation of the exposed distal descending thoracic aortic segment.The distal descending thoracic aortic diameter at 4,8,12 weeks was (0.82±0.13), (1.12±0.43), (1.65±0.58)μm respectively. The control group at 4,8,12 weeks was (0.81±0.04) , (0.94±0.12), (1.09±0.03)μm respectively. The diameter of the ascending aorta (used as an internal control) were not significantly different between groups. Hematoxylin and eosin stained slides showed disruption of the normal elastic lamellar architecture of the CaCl2-exposed aortic wall compared to the contralateral wall or untreated control. Van Gieson-stained sections showed decreased collagen content in the exposed region of aortic wall. Immunohistochemical study indicated significantly more CD3 cells and CD68 cells in the aortas of CaCl2 treated groups than in control aortas. CD3 cells were located in the media and surrounding the vasa vasorum in the adventitia. Conclusion We conclude that abluminal application of CaCl2 to the thoracic aorta reliably produces dilation, wall-thinning, and disruption of mural architecture, the hallmark signs of aneurysm formation. These results suggest that the rat is a useful and technically feasible model for the study of TAAs. To our knowledge, these findings describe for the first time the generation of a reproducible model of isolated TAA formation in SD rat.     

Establishment of simultaneous pancreas and kidney transplantation （SPK） model with cuff technique and portal venous drainage in rats

To establish a simultaneous pancreas and kidney transplantation （SPK） model in the rat. Methods： SD rats served as donors and recipients. The donor portal vein and the recipient superior mesenteric vein were anastomosed and the donor renal veins and recipient renal veins were anastomosed by cuff method. Arterial reconstruction was carried out by end to side anastomosis of the donor abdominal aorta to the recipient abdominal aorta. Enteric drainage was performed by side to side anastomosis between donors＇ duodenum and recipients＇ jejunum. The donor ureter -bladder valve was anastomosed to the bladder of recipients. Results： Out of 30 cases of SPK transplantation, 24 had normal serum glucose and serum creatinine after operation. The successful rate was 80 %. Conclusion： This model of SPK in rats is stable and reliable, which could be applied for further scientific research.     

Response of the xenograft endothelium in the concordant xenotransplantation

Objective: To investigate the response of the xenograft endothelium in the concordant hamster to rat cardiac xenotransplantation and the mechanism of acute vascular rejection. Methods: The animals were divided into 5 groups randomly: control group,CsA group, splenectomy group, D0 splenectomy CsA group and D3 splenectomy CsA group. Hamster heart was heterotopicaly transplanted to rat abdominal cavity. The graft survival was monitored by palpation of the rat abdominal wall. The histological and ultrastructural changes of the xenogafts were investigated. NF-κB and P-selectin expression in the xenograft were detected. Hene Oxigenase-1 and Bcl-2 expression were also detected in the xenografts of different groups. Results: The mean survival time of the xenografts in control group, CsA group, splenectomy group, D0 splenectomy CsA group and D3 splenectomy CsA group was 3.4±0.55, 3.8±0.45, 6.4±1.52, 30 and 7.4±1.14 days. The rejected graft showed typical acute vascular rejection in control group, CsA group,splenectomy group and D3 splenectomy CsA group. Endothelial cells of the rejected xenograft showed dramatic assembly of ribosomes and expansion of the rough endoplasmic reticulum. However, the endothelium of the long-term survived grafts in D0 splenectomy CsA group showed normal architecture. NF-κB and P-selectin expression were detected in the rejected xenografts. HO-1 expression was observed in the long-term survived xenografts in D0 splenectomy CsA group. Conclusion: The endothelial cells of the xenograft might be activated during the acute vascular rejection. Expression of HO-1 might inhibit the upregulation of NF-κB and adhesion molecular which decreases the activation of the endothelium of the graft.     

可溶性成纤维细胞生长因子受体基因转染在抑制慢性排斥所致血管病变中的作用

目的　通过阻断成纤维细胞生长因子 (FGF)作用 ,抑制慢性排斥反应所致血管内膜增生 (AGA)。方法　通过克隆并构建可溶性FGF受体sFGFR 1、cDNA质粒构建腺病毒Adv5 sFGFR 1,转基因载体。体外检测sFGFR 1及FGF 2对STS培养的成纤维细胞增殖抑制作用。采用大鼠腹主动脉转染 5× 10 9pfuAv3 sFGFR 1,分别用等量Av3 Nall及生理盐水做实验及空白对照组。将转染后DA大鼠腹主动脉长约 1 5cm ,原位移植于PVG大鼠体内。于移植后分批定期活杀大鼠 ,取移植腹主动脉进行组织形态学、免疫组化、RT PCR检查 ,观察sFGFR 1表达以及AGA改变。结果　 ( 1)构建sFGFR 1、cDNA质粒可以在大鼠血管内皮细胞获得稳定表达。其分泌型sFGFR 1蛋白可与FGF 2交联并有效抑制FGF 2刺激的培养成纤维细胞的增殖。 ( 2 )体内主动脉移植实验结果显示与空病毒Av3 Nall及生理盐水对照 ,Adv 3 sFGFR 1转染主动脉通过免疫组化及RT PCR显示sFGFR 1基因表达及蛋白分泌。至移植后 90d实验组sFGFR 1转染显著抑制移植主动脉AGA(P =0 0 13)。结论FGF在慢性排斥所致血管病变AGA中具有重要作用。通过sFGFR 1阻断FGF可显著抑制慢性排斥反应所致AGA。     

M2型巨噬细胞在糖尿病小鼠同种异体胰岛移植中的抗排斥作用

目的：探讨腹膜腔来源的M2型巨噬细胞对糖尿病小鼠同种异体胰岛移植的抗排斥作用。方法：体外分 离诱导C57BL/6小鼠腹膜腔M2型和M0型细胞,流式细胞术鉴定巨噬细胞表型。链脲佐菌素(streptozotocin,STZ)诱导 C57BL/6雄性小鼠的糖尿病模型作为受体,分离BALB/c小鼠胰岛细胞移植于C57BL/6糖尿病小鼠左肾包膜下。将移植 后糖尿病小鼠随机分为3组,每组8只。于胰岛移植术后1,3,7 d分别经尾静脉输注PBS(islet+PBS组)、2.5×106个M0型 巨噬细胞(islet+M0组),2.5×106个M2型巨噬细胞(islet+M2组)。移植术后取尾静脉血监测受体血糖水平的变化,记录 胰岛存活时间,并于移植后10 d每组随机抽取2只小鼠处死取左肾做病理学检查,观察移植物形态结构和胰岛素表达 水平。结果：Islet+PBS组、islet+M0组和islet+M2组移植物的中位存活时间分别为6.5(4~10),7.5(4~10)和24(>15) d;与 islet+PBS组和islet+M0组比较,islet+M2组移植物调节血糖正常水平时间和中位存活时间明显延长(P<0.01)。病理学检 查结果显示islet+M2组胰岛移植10 d后移植物结构完整,胰岛素染色阳性;而islet+PBS组和islet+M0组胰岛移植物均被 排斥,胰岛素染色阴性,局部见大量淋巴细胞浸润。结论：腹膜腔来源的M2型巨噬细胞能减轻受体对胰岛移植物的 免疫排斥反应,延长胰岛移植物的存活时间,从而提高受体对血糖的耐受能力。     

Cytomegalovirus infection is associated with cardiac allograft rejection and atherosclerosis

We studied the effects of cytomegalovirus (CMV) infection on 301 cardiac transplant recipients who were treated during the cyclosporine era of immunosuppression (1980 to the present). These patients received varying combinations of cyclosporine, azathioprine, prednisone, rabbit antithymocyte globulin, and OKT3 as their immunosuppressive therapy. Two hundred ten patients were free of CMV infection (non-CMV group). During the same period CMV infection developed in 91 patients, as manifested by a fourfold IgG serologic titer rise, demonstration of CMV inclusion bodies in tissue, or positive cultures for the virus (CMV group). The rate of graft rejection was significantly higher in the CMV group. Graft atherosclerosis was significantly more severe in the CMV group as judged by angiographic criteria or by pathologic study. Patient survival rates were significantly lower in the CMV group. Death caused by graft atherosclerosis was significantly more common among patients in the CMV group. Finally, the graft loss rate (from either death or retransplantation for atherosclerosis) was significantly greater in the CMV group. These data demonstrate that CMV infection in cardiac transplant recipients is associated with more frequent rejection, graft atherosclerosis, and death.     

供肾质量和移植肾急慢性排斥反应关系分析

目的探讨影响供肾质量的因素与术后移植肾发生急、慢性排斥反应的相关性。方法观察87例移植供肾缺血时间、活检组织的光镜表现结合移植后发生急、慢性排斥反应的情况进行分析。结果移植术后跟踪3年．发生移植肾急性排斥反应28例，其中5例(17．8％)有供肾组织有不良改变；慢性排斥反应13例，其中6例(46．1％)有供肾组织有不良改变。采用Logistic回归分析，结果示冷缺血时间、肾小管损伤是急性排斥反应的危险因素；冷缺血时间、肾小球硬化是慢性排斥反应的危险因素，与慢性移植病的发生可能相关。结论提高供肾质量和减少上述的危险因素．对减少肾移植术后急慢性排斥反应的发生是有意义的。     

Studies of CTLA4Ig in acute rejection of pancreas transplantation in rats

INTRODUCTION C ostimulatory pathways between antigen-pre- senting cells (APCs) and T cells have been shown to play a crucial role in T-cell activation and allo-immune responses [1,2]. Among these receptor- ligand pairs, B7/CTLA4-CD28 is one of the two major targets proved to achieve antigen-specific im- munosuppression in experimental organ transplanta- tion[3]. The role of T-cell costimulatory blockade has attracted much attention in various transplantation models [4]. In our study,…     

KSHV编码的趋化因子vMIPII在小鼠异体皮肤移植免疫排斥反应中的作用

目的　重组vMIPII在大肠杆菌中表达及其纯化。观察纯化的vMIPII蛋白对小鼠异体皮肤移植免疫排斥反应的抑制作用。方法　以 pET3 2a为vMIPII克隆基因的表达载体 ,以大肠杆菌BL2 1(DE3 ) plysS为表达菌 ,诱导表达出硫氧还蛋白 vMIPII的融合蛋白 (2 6× 10 3 D)。经金属离子亲和吸附、肠激酶消化以游离vMIPII、阳离子交换层析等步骤纯化目的蛋白。纯化的vMIPII从尾静脉连续 14d注入异体皮肤移植小鼠 (昆明鼠 /Balb/c)。结果　从 1L发酵菌液中可获得高纯度目的蛋白约 4mg。注射vMIPII的异体皮肤移植小鼠组移植皮存活时间较未注射对照组延长 7d。结论　纯化的重组vMIPII对小鼠异体皮肤移植免疫排斥反应有明显的抑制作用 ,能显著延长移植皮的存活时间     

种植受体血管内皮细胞在异种血管移植中的实验研究

To investigate the possible significance and usefulness of reseeding the endothelial cell of recipient for the prevention of hyperacute rejection (HAR) resulting from the xenograft. METHODS: Discordant xenotransplantation model (guinea pig-to-rat) was adopted in this study. Firstly endothelial cells from rat abdominal aorta were separated and cultured. Secondly the guinea pig abdominal aorta of which the endothelium had been removed was cultured with the suspension containing rat endothelial cells (4 x 10(6)/ml). The viability of cultured vessel was assessed using light microscopy and transmission electron microscopy. Thirdly, the guinea pig vessels reseeded with rat endothelial cells were transplanted to rat in vivo. The thrombrosis time was observed. The condition of deposit of IgM and C3 in the recipient's transplanted vessel endothelium was examined by immuno-fluorescence staining assay. RESULTS: The thrombrosis time of the guinea pig vessel reseeded with rat endothelial cells (20.3 + 4.42 h) was significantly prolonged as compared with that of the normal guinea pig vessel (0.35 + 0.284 h) and the guinea pig vessel that had been deprived of endothelium (0.165 + 0.77 h). No deposit of IgM and C3 was seen in the new endothelium of guinea pig vessel in the treated group, whereas deposit of IgM and C3 was observed in the untreated normal guinea pig aorta. CONCLUSION: Donor vessels reseeded with endothelial cells from the recipient will undergo less severe rejection and this technique may be very useful in the attenuation of HAR.     

小剂量抗CD3单克隆抗体治疗肾移植术后早期急性排斥反应的临床研究

目的探讨应用小剂量抗CD3单克隆抗体(OKT3)治疗肾移植术后早期急性排斥反应的效果和安全性.方法将33例发生早期急性排斥反应的肾移植病人分为两组,A组16例(OKT3 5 mg/d);B组17例(OKT3 2.5mg/d).观察排斥反应逆转情况及感染的发生率.结果A组13例(81.25%)急性排斥反应逆转,移植肾功能恢复正常;1例移植肾自发性破裂行移植肾摘除术,2例移植肾失功恢复血液透析.B组15例(88.24%)急性排斥反应逆转,移植肾功能恢复正常;1例移植肾自发性破裂行移植肾摘除术,1例移植肾失功恢复血液透析.两组排斥反应逆转率无显著性差异(P＞0.05).A组合并感染43.75%,B组5.88%;两组比较有显著性差异(P＜0.05).结论小剂量OKT3治疗肾移植术后早期急性排斥反应的效果良好,并发症少,且费用较低.     

诱导抗独特型抗体抑制小鼠移植物排斥反应

目的 探讨抗独特型诱导对小鼠异位心肌移植排斥反应的影响。 Ｃ５７ＢＬ／６小鼠脾细胞免疫ＢＡＬＢ／ｃ小鼠制备抗同种异品系抗体（Ａｂ１）,Ａｂ１交联ＫＬＨ后,免疫ＢＡＬＢ／ｃ小鼠诱导产生抗独特型多克隆抗体（Ａｂ２）,作为受体,观察Ａｂ２对小鼠异位心肌组织移植排斥反应的影响。结果 Ａｂ１交联ＫＬＨ和弗氏佐剂免疫可以有效诱导抗独特型抗体（Ａｂ２）,和对照组相比,Ａｂ２诱导组的小鼠移植物的存活时间明显延长（