目的： 研究丙氨酰谷氨酰胺(A la-Gln) 添加全胃肠外营养(TPN ) 对消化道肿瘤术后化疗患者蛋白质代谢的影响。方法：30 例消化道癌肿患者随机分为两组： 传统组和二肽组，术后给予等热量(每千克体重104 kJ )、等氮量(每千克体重0.16 g)、TPN 同时化疗5 天。手术前后对人体测量、血浆蛋白、淋巴细胞计数等指标进行监测； 术后留24 h 尿测氮平衡和累积氮平衡。结果： 二肽组转铁蛋白(TF)、淋巴细胞数术后第6 天能维持术前水平(P > 0.05)，传统组则明显低于术前(P < 0.05 )； 两组间人体测量、血浆蛋白、淋巴细胞数差异无显著性。术后第6 天传统组累积氮平衡为(- 32。17±10.16) g，二肽组为(- 13.56±5.61) g，两组间每日氮平衡和累积氮平衡差异显著(P < 0.01)。结论：A la-Gln 在肠外营养中的使用是安全有效的，能减轻肿瘤患者术后的分解代谢，有效地改善氮平衡，维持血循环中淋巴细胞的数目，增强对手术及化疗的耐受性。

目的：通过检测IFN-γ基因转染对大肠癌细胞表面抗原的表达情况、对细胞的生长抑制、细胞周期的影响情况，初步探讨IFN-γ基因治疗抗肿瘤作用的机制。方法：制备含人IFN-γ基因的真核表达质粒pcDNA-3-IFN-γ，利用阳离子脂质体将其转染进入人大肠癌细胞株LOVO、SW62O、HCT116BG 及人宫颈癌细胞株Hela，检测基因转染后IFN- γ基因的表达情况，同时检测基因转染对大肠癌细胞CEA、HLA-DR 抗原表达的诱导作用和细胞凋亡及细胞周期的变化。结果：基因转染后，原来高表达CEA 的细胞株(LOVO、HCT116BG)其上清中CEA含量增加明显(从21.25±6.76 μ/l增加到34.96±7.07 μg/l P <0.05)，而原来低表达甚至不表达CEA的细胞株(Hela、SW620)其上清CEA含量则无明显增加 (P >0.05)。各细胞株表面的HLA-DR 的表达量在导入IFN- γ基因后明显增强(平均表达率从3.91±3.61 % 增加到11.67±7.20 % P <0.01)。通过对细胞的凋亡情况和细胞周期的变化显示：转染IFN-γ基因后促进了LOVO细胞的凋亡(各时段平均凋亡率对照组与治疗组分别为8.27±5.62 %与15.32±11.41% P <0.05)，细胞的S 期比例随作用时间延长而呈逐渐降低趋势，显示了基因转染后DNA的合成代谢受到抑制。结论：IFN-γ基因转染后可有效增强大肠癌细胞表面抗原的表达，诱导机体产生抗肿瘤免疫应答；并可能通过抑制细胞DNA的合成，促进细胞的凋亡，抑制肿瘤细胞的增生等机制发挥抗肿瘤作用。

AIM: To evaluate the local expression of CTLA4 Ig gene in small bowels and its effect on preventing acute rejection of the small bowel allografts. METHODS: Groups of Wistar rats underwent heterotopic small bowel transplantation from SD rats. The recipients were randomly divided into experimental group (allografts were transfected with CTLA4Ig gene) and control group (non CTLA4Ig gene transfected). In the experimental group, the donor small bowels were perfused ex vivo with CTLA4Ig cDNA packaged with lipofectin vector via intra-superior mesenteric artery before transplantation, and the CTLA4Ig expression in the small bowel grafts post-transplantation was assessed by immunohistology. On d 3, 7 and 10 posttransplantation, the allografts in each group were harvested for the examination of histology and detection of apoptosis. RESULTS: Small bowel allografts treated with CTLA4Ig Cdna showed abundant CTLA4Ig expression after transplantation. Acute rejection of grade I on d 7 and grade II on d 10 after transplantation was noticed in the control allografts, and a dramatically increased number of apoptotic enterocytes in parallel to the progressive rejection could be recognized. In contrast, the allografts treated with CTLA4Ig cDNA showed nonspecific histological changes and only a few apoptotic enterocytes were found after transplantation. CONCLUSION: Local CTLA4Ig gene transfection of small bowel allograft is feasible, and the local CTLA4Ig expression in the allograft can prevent acute rejection after transplantation.

In order to facilitate preclinical research, we established a new combined liver-small bowel transplantation rat model. Male inbred Wistar rats were chosen as donors and recipients. An en bloc liver-small bowel graft was harvested. During the donor operation, the inferior vena cava in the chest was removed to be used as an interpositional venous graft to anastomose to the portal vein. In the recipient operation the portal veins of donor and recipient were quickly anastomosed using a cuff technique instead of the traditional suture method. Rearterialization was achieved by anastomosing the superior mesenteric artery of graft to the right renal artery of the recipient. The recipient small bowel was resected and intestinal continuity restored simultaneously by two end-to-end anastomoses. The postoperative 5-day survival rate was 77.5% (31/40) and 60-day survival rate, 72.5% (29/40). Recipient rats that tolerated the operation remained healthy. Liver and renal function was normal. The liver and intestinal grafts showed normal histological architecture in all rats surviving for 2 months postoperatively. Our results demonstrated that the present model is feasible, allowing preclinical experimental research on combined liver-small bowel transplantation.

Dendritic cells (DC) constitute a complex system of uniquely specialized antigen-presenting cells (APC) that play crucial roles in the initiation and regulation of immune responses. Recent studies have demonstrated that DC silenced by siRNA IL-12 p35 showed tolerogenic capacity in vitro. However, their mechanism of action is not fully understood. In this study, IL-12p35 siRNA was chemically synthesized and transfected into DCs. A coculture of T cells and DCs was performed. After 30 min coculture, T cells were harvested and analyzed. We showed that the IL-12 p35 silenced DCs decreased IL-12-induced T cell responses through blocking tyrosine phosphorylation of JAK2, TYK2, STAT3, and STAT4 proteins in T cells. These results demonstrate IL-12 p35 silenced DCs modulate immune responses by blocking IL-12 signaling through JAK-STAT pathway in T cells.