Collagen membrane alleviates peritendinous adhesion in the rat Achilles tendon injury model / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Tendon adhesion is one of the most common causes of disability following tendon surgery. Therefore, prevention of peritendinous adhesion after surgical repair of tendon is a major challenge. The aim of this study was to explore the possible application of a collagen membrane for the prevention or attenuation of peritendinous adhesions.</p><p><b>METHODS</b>Sprague-Dawley (SD) rat Achilles tendon was cut and sutured by a modified Kessler's technique with or without the collagen membrane wrapped. Macroscopic, morphological and biomechanical evaluations were applied to examine the recovery of the injured tendon at 4 and 8 weeks after surgery.</p><p><b>RESULTS</b>The surgery group wrapped by collagen membranes had a better outcome than the group with surgery repair only. In the collagen membrane-treated group, less adhesion appeared, stronger tensile strength was detected, and more tendon fibers and collagen I expression were observed morphologically.</p><p><b>CONCLUSION</b>Wrapping the tendon with a collagen membrane may be an efficient approach for tendon repair and preventing tendon adhesion after its ruptures.</p>

Blockade of 4-1BB/4-1BB ligand interactions prevents acute rejection in rat liver transplantation / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Blocking the 4-1BB/4-1BB ligand (4-1BBL) signal may modulate the secretion of Th1/Th2 cytokines and prolong the survival of the grafts, which play a key role in organ transplantation tolerance. The aim of this study was to investigate the role of blockade of the 4-1BB/4-1BBL co-stimulatory pathway with 4-1BBL monoclonal antibody (mAB) in acute rejection of rat orthotopic liver transplantation.</p><p><b>METHODS</b>The orthotopic liver transplantation model was set up, while male Lewis rats were used as liver donors and Brown-Norway rats as recipients. The recipient rats were intravenously injected with anti 4-1BBL mAB or isotype control antibody. Groups were monitored for graft survival after transplantation. Plasma chemistry, including aspartate transaminase (AST), alanine aminotransferase (ALT), and bilirubin (BIL), was assayed. The concentrations of interleukin (IL)-2, IL-10 and interferon (IFN)-gamma in plasma were also measured by enzyme-linked immunosorbent assay. Allograft histology images were collected under light microscope and electron microscope.</p><p><b>RESULTS</b>Isotype antibody treated recipients exhibited elevated plasma levels of liver injury markers including AST, ALT and BIL, progressive portal and venous inflammation and cellular infiltration of the liver allografts, and a mean graft survival time (MST) of 10.9 days. Administration of anti 4-1BBL mAB resulted in a decrease in plasma levels of liver injury markers and the concentrations of IL-2, IL-10 and IFN-gamma. The histological grade of rejection on day 7 decreased and MST (17.3 days) increased substantially.</p><p><b>CONCLUSIONS</b>These results demonstrate that attenuation of acute rejection follows the blockade of the 4-1BB/4-1BBL co-stimulatory pathway with 4-1BBL monoclonal antibody and strongly suggest it is a promising strategy to prevent progression of graft rejection by suppressing T cell-mediated immunity.</p>

RASSF1A expression inhibits cell growth and enhances cell chemosensitivity to mitomycin in BEL-7402 hepatocellular carcinoma cells / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>The antitumor role of Ras association domain family 1A (RASSF1A) gene and its potential molecular mechanisms are not well understood. The objective of this study was to observe the antitumor ability of RASSF1A in hepatocellular carcinoma, and study the mechanisms of cell apoptosis induced by RASSF1A.</p><p><b>METHODS</b>After stably transfecting a RASSF1A (wild-type or mutant) expression vector into the BEL-7402 hepatocellular carcinoma cell line, RT-PCR and Western blotting was used to detect the RASSF1A expression levels in recombinant cells. The effects of wild-type RASSF1A on cell growth were observed in vitro by analyzing cell proliferation rate, cell colony formation, and in vivo by analyzing tumorigenesis in nude mice. In addition, the effect of RASSF1A gene expression on the chemosensitivity of human hepatocellular carcinoma cells to antitumor drugs was examined by inhibition of cell proliferation and the percentage of apoptotic cells.</p><p><b>RESULTS</b>Wild-type RASSF1A, not the mutant, suppressed cell growth in vitro and in vivo. Re-expression of wild-type RASSF1A could enhance the inhibition of cell proliferation and the percentage of apoptotic cells following cell treatment with mitomycin, but had no significant effect when combined with adriamycin, etoposide, 5-fluorouracil and cisplatin treatment.</p><p><b>CONCLUSION</b>Wild-type RASSF1A inhibits cell growth and enhances cell chemosensitivity to mitomycin in hepatocellular carcinoma, suggesting that RASSF1A may serve as a new target for gene therapy in hepatocellular carcinoma patients.</p>