Colorectal Neoplasms ; pathology ; Humans ; Neoplasm Staging

Humans ; Practice Guidelines as Topic ; Rectal Neoplasms ; surgery

Humans ; Rectal Neoplasms ; pathology ; surgery ; Rectum ; surgery

Objective To explore the mechanism of delayed xenograft rejection(DXR) by dynamic observation of histological and immunohistologic changes in mouse-to-rat cardiac xenografts.Methods A model of mouse-to-rat cardiac heterotopic xenotransplantation in neck was established by cuff technique.NIH mouse hearts not transplanted served as controls(n=4).Some xenograft recipients were killed and cardiac xenografts harvested at end of 3,8,16,24 h(n=4 for each time point) after transplantation.The cardiac hearts(n=16) of some xenograft recipients were not harvested until rejection time to determine their survival time.All heart samples were examined by HE and immunohistochemistry for semi-quantitative determination of antibodies including C3,IgM,IgG,E-selectin and macrophage marker——CD68.Results During the period after transplantation,the degree of rejection of xenografts became more and more serious till ultimate rejection.The mean survival time of the xenografts was(49.3?16.2) h.Immunohistochemical examination showed C3 were not detected in the xenografts at any time during the course of rejection;From 3 h after transplantation,obvious deposition of IgM was found in the grafts and IgG deposition got abundant;E-selectin expression was found as early as 3 h after transplantation and increased gradually;There was progressive infiltration by macrophages in the grafts.Conclusion Mouse-to-rat cardiac xenotransplantation can serve as an animal model of DXR.Endothelial cells activation,IgM and IgG,macrophage infiltration involve in DXR development except C3.

Multilocus sequence typing MLST with high solution sensitivity and specificity is widely used to study the population genetic structure of pathogen by amplification and sequencing of the housekeeping genes. MLST also provides more evidence and plays an important role in parasite research. This paper reviews the principle and method of MLST and its applica-tion on population genetic structure analysis of parasites.

Objective To investigate the protective effect of heme oxygenase-1 for xeno-heart transplantation and the possible mechanism.Methods Cobalt protoporphyrin (CoPP), HO-1 inducer, and zinc protoporphyrin (ZnPP), HO-1 inhibitor, were used to intervene donors and recipients on the model of NIH-Wistar cardiac transplants respectively and simultaneously some of recipients were treated with immunesuppressor cyclosporine A (CsA), and control group and CsA treated group were set up respectively. The expression of HO-1 protein, HO-1 mRNA, caspase-3 and STAT-3 in transplanted heart tissue was detected by immunohistochemistry, RT-PCR and Western Blot. At the same time, HO-1 enzymatic activity was examined in heart tissue, and the cardiac cell apoptosis was examined by means of TUNEL. The differences among various factors were compared.Results The survival time of cardiac transplants in CoPP group was longer than that in control and ZnPP groups (P

Objective To investigate the influence of the aberrant protein expression and mRNA transcription of transforming growth factor ? 1(TGF? 1) on the biological behavior of human bladder transitional cell carcinomas. Methods The expression of TGF? 1 was investigated in 74 specimens of TCCs by SP immunohistochemistry staining, and the level of TGF? 1 mRNA were determined in 43 cases of TCCs by the method of quantitative RT PCR. Results The positives expression rate of TGF? 1 was 89.2%. Superficial tumors had lower overexpressive rate of TGF? 1(33.3%) than the invasive TCCs(83.8%), P

Combined Modality Therapy ; Evidence-Based Medicine ; Humans ; Rectal Neoplasms ; therapy

Colorectal Neoplasms ; drug therapy ; pathology ; therapy ; Humans ; Pathology, Clinical ; organization & administration ; standards

Objective High mobility group box-1 protein ( HMGB1) plays an essential role in regulating energy metabolism of tumor cells via affecting mitochondrial autophagy .The aim of this study was to explore the effect of HMGB 1 on mitochondrial biogene-sis and cell energy metabolism in anoxia environment . Methods HepG2 cells were divided into normoxia control group ( cells were cultured in a culture box containing 5%CO2) , hypoxia control group ( cells were cultured in a culture box containing 1%O2+5%CO2+94%N2 ) , hypoxia HMGB1 siRNA group ( cells were cultured in a culture box containing 1% O2+5% CO2+94% N2 after transfected with HMGB1 siRNA) and hypoxia NC siRNA group ( cells were cultured in a culture box containing 1%O2+5%CO2+94%N2 after trans-fected with negative control siRNA ) .MTS assay was carried out to measure cell proliferation rate .The alterations of mitochondrial bio-genesis associated proteins were detected by RT-PCR and western blot.Mitochondrial density and morphology were determined by transmission electron microscopy (TEM).The ATP content in whole cell extracts was determined with a colorimetric ATP detection kit . Results Compared with the hypoxia control and hypoxia NC siR-NA group, the proliferationof hypoxia HMGB1 siRNA group was significantly inhibited, especially in 48 h and 72 h(P<0.05).Com-pared with hypoxia control group and hypoxia NC siRNA group , the expression of PGC 1α, NRF1and TFAM in hypoxia HMGB1 siRNA group were decreased significantly ( P<0.05) .Western blot results showed that , compared with normoxia control group , the expressions of PGC1α(0.494±0.210 vs 0.090±0.020), NRF1(1.080±0.470 vs 0.581±0.190)and TFAM(1.585±0.340 vs 0.792±0.350) protein in hypoxia 24 h group were increased obviously ( P<0.05) .Compared with hypoxia control group and hypoxia NC siRNA group , the expres-sions of PGC 1α, NRF1 and TFAM protein in hypoxia HMGB1 siRNA group were significantly decreased (P<0.05).Compared with hypoxia control group , the content of ATP in the HMGB 1 siRNA hypoxia group was significantly decreased , and hypoxia 12 h and 24 h were the most obvious ( P<0.05) . Conclusion HMGB1 could maintain cell energy metabolism by regulating mitochondrial biogene-sis so that cells could continue to proliferate in adverse anoxia environment .