Ultrastructure study on patients with spontaneous rupture of hepatocellular carcinoma / 中华外科杂志

<p><b>OBJECTIVE</b>To investigate the ultrastructure of small artery wall in patients with spontaneous rupture of hepatocellular carcinoma (HCC).</p><p><b>METHODS</b>Transmission electron microscopy was used to study 11 specimens from ruptured HCC and 11 cases with non-ruptured HCC.</p><p><b>RESULTS</b>The phenomenon of activated phagocytosis in macrophage could be found in 3 cases with ruptured HCC and 10 cases with non-ruptured HCC, respectively (P < 0.05). In 9 specimens with ruptured HCC, the evidence of vascular injury characterized as less cell junctions and larger fenestrae in endothelial cells, broken elastic lamina, proliferated and fragmented elastin and damaged structure of collagen was found in small arteries. The phenomenon of electron-dense deposit in the elastic lamina, and signs of more protein synthesis in endothelial cells were also present in these specimens. In the patients with non-ruptured HCC, the evidence of vascular injury can be found only in 2 cases (P < 0.01). Less cell junctions and larger fenestrae could increase the permeability of vascular wall. The electron-dense deposition in elastic lamina may represent the deposition of antigen-antibody complex in elastic membrane which had been found in our previous study. The vascular injury was postulated to be caused by the deposition of antigen-antibody complex in vascular wall which was identified by our previous study. The vascular wall in the patient with ruptured HCC could become stiff and weak due to the proliferated fragment elastin and damaged collagen which would make the blood vessels more prone to splitting and result in hemorrhage and the rupture of HCC.</p><p><b>CONCLUSIONS</b>The vascular injury caused by antigen-antibody complex deposition might related to the spontaneous rupture of HCC.</p>

Mechanism of spontaneous rupture of hepatocellular carcinoma / 中华外科杂志

<p><b>OBJECTIVE</b>To study the mechanism of spontaneous rupture of hepatocellular carcinoma (HCC).</p><p><b>METHODS</b>The specimens of 30 patients with ruptured HCC and 30 patients with non-ruptured HCC were collected. Immunofluorescence, immunohistochemical and flow cytometry techniques were used to detect the phagocytosis of macrophages and the deposition of immune complex (IC) on vascular wall.</p><p><b>RESULTS</b>In this study, the poor function of macrophage phagocytosis was found in patients with ruptured HCC, which could results in the cumulating of IC and deposition on vascular wall. The IC, which composed of hepatitis B virus e1 antigen (HBeAg/1), complement C1q and immunoglobulins, was found deposited in the elastic membrane of arteries. Likely as a result of IC deposition, vascular injury occurs mainly in the small arteries where the deposition of IC was present. As the small arteries were the blood vessels with predominant injury, they would likely to be the ones to split and cause hemorrhage and rupture of HCC during vascular load increase.</p><p><b>CONCLUSIONS</b>We would conclude that the poor function of macrophage phagocytosis, which lead to the IC deposition and vascular injury may be the factors involved in the pathogenesis of ruptured HCC.</p>

The role of IL-15 in the process of acute rejection in liver and heart transplantation in rats / 中华外科杂志

<p><b>OBJECTIVE</b>To study the real effect of IL-15, a kind of T lymphocyte activators which were derived from lymphocytes, on the acute rejection process in heart and liver transplantation in rats.</p><p><b>METHODS</b>Male (body weight 200 - 250 g) 1A (RT1(a)) and LEW (RT1(l)) rats were selected as donors and recipients, respectively. Heterotopic heart transplantation (in abdomen) and orthotopic liver transplantation were performed as the acute rejection model group (experimental group); LEW (RT1(l))-->LEW (RT1(l)) as donors and recipients to establish isografts transplantation as the control group. Animals were sacrificed on day 1, 3, 5, 7 and graft specimens were collected. Microarray, immunohistochemistry and Western-blotting methods were used to detect the expressions of IL-15, IL-2 and IFN-gamma, etc. 48 rats were divided evenly into two groups and each time-point consisted of 6 rats.</p><p><b>RESULTS</b>Acute rejections which were clarified by pathological findings and animal manifestations were found 3 days after operation in the experimental group. The early expression of IL-15 was found on endothelial cells in allografts 1 day after operation in contrast to IL-2, which expressed lately and only be found on inflammatory cells including lymphocytes and Kupffer cells 3 days after graft implantation. The result of INF-gamma was the same as that of IL-2.</p><p><b>CONCLUSIONS</b>IL-15 appeared earlier in heart and liver allografts than IL-2 and IFN-gamma in rat acute rejection model, and the expression site differed from the later two. IL-15 participated in acute rejection reaction earlier in this process and the pathway may be different from IL-2 and IFN-gamma. Early blocking this pathway combined with other blockade would have a promising result in control of the progression of acute rejection.</p>