Objective To investigate morbidity, mortality and survival of patients with adenocarcinoma of the pancreas who underwent pancreaticoduodenectomy with en bloc portal vein resection, and to evaluate its effect on radical resection of pancreatic carcinoma. Methods Between 1999 and 2003, 32 patients with ductal adenocarcinoma of the head of the pancreas who underwent pancreaticoduodenectomy with SMPV resection were retrospectively analyzed. Patients were divided into two groups with group A(n = 12) in which the wall of portal vein was surrounded by carcinoma without true invasion,and group B(n = 20) , by tumor transmural invasion. Results The overall morbidity was 31% , there was no operative mortality, the 1,3-year survival rate was 59% and 22% respectively. The mean survival time of patients with microscopically positive margin was 5. 6 months as compared with 20 months with microscopically negative margin. There was no difference in tumor size, margin positivity, nodal positivity, and 1,3-year survival rate between the two groups. Conclusions Pancreaticoduodenectomy combined with SMPV resection can be performed safely, without increasing the morbidity and mortality. SMPV resection should be performed only when a margin-negative resection is expected. SMPV invasion is not associated with histologic parameters suggesting a poor prognosis.

Objective To induce islet allograft long-term survival through cotransplantation of islet cells with sertoli cells. Methods Testicular sertoli cells were prepared by digestion with collagenase, trypsin and DNase, and were cultured for 48 hours. Collagenase digested and Ficoll purified donor (Wistar rat) islets were cotransplanted with allogeneic sertoli cells in the absence of systemic immunosuppression. Terminal leoxynucleotidyl transferase-mediated X-dUTP nick-end labeling (TUNEL) was used to label apoptosis of lymphocytes surrounding the islet graft. Results Cotransplantation of islets and 1 × 107 sertoli cells reversed the diabetic state for more than 60 days in 100% (6/6) of the chemically diabetic Sprague Dawley rats. Grafts consisting of islets alone or islets plus 1 × 105 sertoli cells survived only for 5 - 6 days. Apoptosis of lymphocytes surrounding the islets was quite clear. Conclusion Cotransplantation of islets with FasL+ sertoli cells induces local immune privilege and allows long-term graft survival without systemic immunosuppression.

Macrophages show significant heterogeneity in function and phenotype, which could shift into different populations of cells in response to exposure to various micro-environmental signals. These changes, also termed as macrophage polarization, of which play an important role in the pathogenesis of many diseases. Numerous studies have proved that Hesperidin (HDN), a traditional Chinese medicine, extracted from fruit peels of the genus citrus, play key roles in anti-inflammation, anti-tumor, anti-oxidant and so on. However, the role of HDN in macrophage polarization has never been reported. Additional, because of its poor water solubility and bioavailability. Our laboratory had synthesized many hesperidin derivatives. Among them, hesperidin derivatives-12 (HDND-12) has better water solubility and bioavailability. So, we evaluated the role of HDND-12 in macrophage polarization in the present study. The results showed that the expression of Arginase-1 (Arg-1), interleukin-10 (IL-10), transforming growth factor β (TGF-β) were up-regulated by HDND-12, whereas the expression of inducible Nitric Oxide Synthase (iNOS) was down-regulated in LPS- and IFN-γ-treated (M1) RAW264.7 cells. Moreover, the expression of p-JAK2 and p-STAT3 were significantly decreased after stimulation with HDND-12 in M1-like macrophages. More importantly, when we taken AG490 (inhibitor of JAK2/STAT3 signaling), the protein levels of iNOS were significantly reduced in AG490 stimulation group compare with control in LPS, IFN-γ and HDND-12 stimulation cells. Taken together, these findings indicated that HDND-12 could prevent polarization toward M1-like macrophages, at least in part, through modulating JAK2/STAT3 pathway.
Animals ; Cytokines ; genetics ; metabolism ; Enzyme Inhibitors ; pharmacology ; Gene Expression Regulation ; drug effects ; Hesperidin ; chemistry ; pharmacology ; Inflammation ; genetics ; metabolism ; Janus Kinase 2 ; antagonists & inhibitors ; metabolism ; Macrophages ; drug effects ; immunology ; metabolism ; Medicine, Chinese Traditional ; Mice ; Molecular Structure ; Phosphorylation ; drug effects ; RAW 264.7 Cells ; STAT3 Transcription Factor ; antagonists & inhibitors ; metabolism ; Signal Transduction ; drug effects