0.05). Conclusion CD105 overexpression may play a crucial role in early recurrence of HCC in patients after operation. The expression of CD105 mRNA in the tumor peripheral tissue was much higher than in the tumor center and normal liver tissue, which indicated CD105 was related to early recurrence.

Objective To investigate the relevant factors for fungal infection following pancreatoduodenectomy and offer the theoretical foundation for preventing the emergence of complications after operation. Methods Medical records from 562 consecutive patients who underwent pancreatoduodenectomy in this hospital from 1995 to 2005 were retrospectively reviewed by using single factor and non-condition Logistic regression analyse. Results ①Seventy-eight patients (13.9%) developed invasive fungal infection. The most frequently isolated fungal were Candida albicans accounted for 67.0%, and followed by Candida glabrata, Candida papasilosis and Candida tropicalis and gastrointestinal tract was the most common infection site, followed by respiratory tract, abdominal cavity. ②Fungal infection occurred significantly more often in patients with the length of time in parenteral nutrition, antibiotic use or abdominal cavity complications. Conclusion The most common infection site and isolated fungal associated with pancreatoduodenectomy were gastrointestinal tract and Candida albicans. Abdominal cavity complications such as pancreatic fistula, biliary fistula and abdominal infection and extended use parenteral nutrition and antibiotic are the most important factors leading to invasive fungal infection after pancreatoduodenctomy. Eliminating the various risk factors will decrease the incidence of fungal infection.

Objective To study on the results of magnifying endoscopy in gastric atrophy, intestinal metaplasia (IM) and dysplasia, and evaluate their feasibility and accuracy for the diagnosis of these lesions. Methods One hundred patients were examined by magnifying endoscopy, Fujinon EG485 ZH modal, and stained with 0. 5% methylene blue. After defining magnifying endoscopic patterns of gastric pits as types A, B, C, D, and E, the diagnostic classification and endoscopic criteria were developed for the diagnosis of atrophy, IM and dysplasia. The results of 417 histopathological biopsy specimens taken from the corresponding areas of gastric mucosa under magnifying endoscopy were regarded as gold standard. Results Sparse and thick gastric pits mainly appeared in gastric atrophy, IM mainly appeared in gastric mucosa of type C, type D, and type E with positive stain, dysplasia appeared as depressed, slightly raised, or flat mucosa accompanied by loss of clear pattern, fine pits or coarse and irregular microstructure. The sensitivity and specificity of magnifying endoscopies in the diagnosis of atrophy, IM and dysphasia were 95. 85% , 95. 09% ; 88. 30% , 90.83% ; and 91.52% , 94. 41% respectively, all were higher than those of routine endoscopy. Conclusion The diagnostic accuracy significantly increased as depending upon the morphological features of gastric atrophy , IM, or dysplasia under magnifying endoscopy.

Objective To investigate the effects of inhibiting TIM-4 function in Kupffer cells (KCs) on liver graft rejection in mice and explore the underlying mechanism. Methods Mouse models of orthotopic liver transplantation were treated with a control mAb group and TIM-4 mAb. The activated KCs were assayed with immunohistochemistry after operation. The expression of TIM-4 in KCs were assayed with Western blotting and RT-PCR and the levels of AST, ALT, TBIL, TNF-α, IFN-γand CCL2 were assayed detected. The expression of TIM-4 in KCs was observed with laser confocal microscopy. HE staining was used to observe the microstructure of the liver tissues, and the number of CD25 +Foxp3 +T cells was determined using with flow cytometry; the proteins levels of p-P65and p-P38 were assayed with Western blotting. The donor mice were treated with clodronate liposomes to destroy the KCs in the liver before transplantation, and the liver grafts were examined for graft rejection. Results The number of activated KCs in the liver graft increased progressively over time. Compared with the sham-operated group, the liver graft showed significantly increased TIM-4 protein and mRNA levels at 1, 3, and 7 days after transplantation (P<0.05) and increased levels of AST, ALT, TBIL, TNF-α, IFN-γ and CCL2 at 7 days (P<0.05). The graft in TIM-4 mAb group showed mild pathological changes with a mean RAI score of 2.67 ± 0.75, which was significantly lower than that in control mAb group (P<0.05). The mean survival time of the recipient mice was 53.8±6.4 days in TIM-4 mAb group, significantly longer than that in the control mAB group (14.5±2.9 days, P<0.05). Donor treatment with clodronate liposomes resulted in comparable RAI scores in TIM-4 mAb and control mAb groups (8.01±0.64 vs 7.93±0.56, P>0.05). Theprotein levels of p-P65 and p-P38 in TIM-4 mAb group were significantly lower than those in control mAb group (P<0.05), and CD25+Foxp3+T cells in the liver graft increased significantly in TIM-4 mAb group. Conclusion Inhibition of TIM-4 function in KCs reduces the production of inflammatory factors after liver transplantation possibly by inhibiting the NF-κB and MAPK signaling pathways and promoting the proliferation of Foxp3+Treg cells to induce allograft tolerance.

Objective To investigate the effects of inhibiting TIM-4 function in Kupffer cells (KCs) on liver graft rejection in mice and explore the underlying mechanism. Methods Mouse models of orthotopic liver transplantation were treated with a control mAb group and TIM-4 mAb. The activated KCs were assayed with immunohistochemistry after operation. The expression of TIM-4 in KCs were assayed with Western blotting and RT-PCR and the levels of AST, ALT, TBIL, TNF-α, IFN-γand CCL2 were assayed detected. The expression of TIM-4 in KCs was observed with laser confocal microscopy. HE staining was used to observe the microstructure of the liver tissues, and the number of CD25 +Foxp3 +T cells was determined using with flow cytometry; the proteins levels of p-P65and p-P38 were assayed with Western blotting. The donor mice were treated with clodronate liposomes to destroy the KCs in the liver before transplantation, and the liver grafts were examined for graft rejection. Results The number of activated KCs in the liver graft increased progressively over time. Compared with the sham-operated group, the liver graft showed significantly increased TIM-4 protein and mRNA levels at 1, 3, and 7 days after transplantation (P<0.05) and increased levels of AST, ALT, TBIL, TNF-α, IFN-γ and CCL2 at 7 days (P<0.05). The graft in TIM-4 mAb group showed mild pathological changes with a mean RAI score of 2.67 ± 0.75, which was significantly lower than that in control mAb group (P<0.05). The mean survival time of the recipient mice was 53.8±6.4 days in TIM-4 mAb group, significantly longer than that in the control mAB group (14.5±2.9 days, P<0.05). Donor treatment with clodronate liposomes resulted in comparable RAI scores in TIM-4 mAb and control mAb groups (8.01±0.64 vs 7.93±0.56, P>0.05). Theprotein levels of p-P65 and p-P38 in TIM-4 mAb group were significantly lower than those in control mAb group (P<0.05), and CD25+Foxp3+T cells in the liver graft increased significantly in TIM-4 mAb group. Conclusion Inhibition of TIM-4 function in KCs reduces the production of inflammatory factors after liver transplantation possibly by inhibiting the NF-κB and MAPK signaling pathways and promoting the proliferation of Foxp3+Treg cells to induce allograft tolerance.

OBJECTIVE To study the osteoprotective effects and possible mechanism of total saponins of Chaenomeles speciosa on rheumatoid arthritis （RA） model mice， and to provide reference for further development of anti-RA drugs. METHODS Seventy male DBA/1 mice were randomly divided into normal group， model group， low-dose and high-dose groups of C. speciose total saponins （60， 240 mg/kg）， Tripterygium wilfordii polyglycoside tablets group （positive control， 30 mg/kg）， with 14 mice in each group. In addition to the normal group， the other groups of mice were induced by glucose-6-phosphate isomerase mixed polypeptide to prepare RA model. The body weight， rear toes thickness and arthritis scores of each group were recorded； the synovial inflammation， bone and cartilage destruction of ankle joint tissues were observed by hematoxylin-eosin staining， tartrate- resistant acid phosphatase staining and safranin O-fast green staining； the contents of interleukin-6 （IL-6） in serum and tumor necrosis factor α （TNF-α）， IL-4 and IL-10 in ankle joint tissues were detected by ELISA； the expression levels of receptor activator of nuclear factor-κB ligand （RANKL）， receptor activator of nuclear factor-κB （RANK）， osteoprotegerin （OPG）， tumor necrosis factor receptor-associated protein 6 （TRAF6） and nuclear factor of activated T cells 1 （NFATC1） protein in ankle joint tissues were detected by Western blot assay. RESULTS At the end of administration， compared with normal group， the body mass of mice in the model group was significantly reduced （P＜0.05）， and the arthritis score and the thickness of the left and right rear toes were significantly increased （P＜0.05）； the ankle joint tissues of mice in the model group showed significant synovial proliferation and inflammatory infiltration， the number of osteoclasts increased significantly and significant destruction of cartilage tissue. The content of IL-6 in serum， the content of TNF-α， the protein expression levels of RANKL， RANK， TRAF6 and NFATC1 in the ankle joint tissues were increased significantly （P＜0.05）， while the contents of IL- 4 and IL-10， the protein expression level of OPG in the ankle joint tissues were decreased significantly （P＜0.05）. Compared with model group， above pathomorphological changes and the content/level of indicators of mice in each administration group were significantly improved （P＜0.05）. CONCLUSIONS Total saponins of C. speciosa may exert osteoprotective effects on RA model mice， the mechanism of which may be associated with reducing the contents of IL-6 and TNF-α， increasing the contents of IL-4 and IL-10， inhibiting the activation of RANKL/RANK/OPG signal pathway， thus inhibiting the proliferation of osteoclasts and promoting the repair of cartilage and bone tissue.

Rheumatoid arthritis （RA） is a systemic chronic auto-inflammatory disease， characterized by infiltration of inflammatory cells， pannus formation， articular cartilage destruction， and bone matrix destruction. Therefore， improving articular cartilage destruction has an important impact on the treatment of RA. Chinese medicine has a good application effect in improving cartilage destruction of RA due to its characteristics of multiple components， multiple targets， high activity and low side effects. Based on this， the author reviewed relevant literature to summarize the relevant research and mechanism of Chinese medicine and its active components in improving RA cartilage destruction. The results showed that Chinese medicine and its active components can improve RA cartilage destruction by regulating inflammatory factors， phosphatidylinositol 3-kinase/protein kinase B， Wnt/β- catenin， nuclear factor-κB， mitogen-activated protein kinase， Janus kinase 2/signal transduction and activator of transcription 3/ vascular endothelial growth factor， microRNAs， fibroblastic synovial cells.