[Study on the three dimensional hepatic virtual operation based on the data of 64-slice helical CT scanning].

OBJECTIVE: To study the surgery plan and simulation effect of the three dimensional (3D) hepatic virtual operation based on the data of 64-slice helical CT scanning and to probe the feasibility of the virtual operation based on the FreeForm Modeling System. METHODS: The volunteer liver was scanned to collect two dimensional (2D) DICOM data of 64-slice helical CT scanning and the 3D hepatic and intrahepatic vessels model were reconstructed by MIMICS software. The reconstructed liver, the intrahepatic vessels model and the artificial tumor models were output into the FreeForm Modeling System in the STL format. The device PHANTOM with the characterization of dynamo-feedback was applied to make the operation on the 3D hepatic. RESULTS: The spatial relationship between the tumour and the intrahepatic vessels were clearly observed by rotation and enlargement of the target. According to the operation principle, the left lobe of liver resection was simulated by manipulating the device PHANToM. Through the liver transparence surface, the intrahepatic vessels were easily distinguished. The operation procedure was accord with the clinic hepatic surgery. Meanwhile, during the operation, by adjusting the incision objective intensity, the dynamo-feedback intensity was definitely touched. CONCLUSIONS: By using the FreeForm Modeling System,the hepatic operation procedure can be simulated ahead of time. The operation complication in the practical surgery can be anticipated and the individualization operation schema can be reasonable instituted.

[Image segmentation and three-dimensional reconstruction of the liver based on 64-slice spiral CT scanning data].

OBJECTIVE: To study the segmentation methods of the liver CT images and the value of 3-dimensional (3D) reconstruction of the liver in the planning of hepatic surgery. METHODS: The 2D Digital Imaging and Communications in Medicine (DICOM) format data of the liver obtained from healthy volunteers were transformed into bmp format image, and the liver image segmentation was performed using Photoshop software. The 3D model was reconstructed using MIMICS software. RESULTS: The DICOM format data of the liver obtained by 64 slice spiral CT included totally 658 slice images. The segmented liver image showed clear profiles and complete intrahepatic duct data were reserved. The segmented liver images were free of discontinuation during continuous observation. The liver surface and internal ductal system, including the hepatic arteries and veins, and the hepatic portal system and their branches, were represented clearly. The reconstructed liver allowed clear identification of the anatomic landmark and matched the actual liver volume. The reconstructed ductal structure were distinct and continuous with natural texture. The reconstructed liver and the hepatic internal duct system were simultaneously displayed by adjusting the transparency of the liver, and the blood vessels were also represented. CONCLUSION: Segmentation of the liver images in different phases using Photoshop can be feasible for liver reconstruction. The reconstructed liver and the intrahepatic ductal structure allow vivid 3D observation of the spatial relationship among the major tracts and accurate estimation of the liver volume.

[Expressions and role of endogenetic matrix metalloproteinases-9 and transforming growth factor-beta during wound healing of blast injury].

OBJECTIVE: To investigate the expression of endogenetic matrix metalloproteinases-9 (MMP-9) and transforming growth factor-beta(TGF-beta) and their role in the wound healing of blast injury. METHODS: Rat models of blast injury under a humid and hot environment were established and the effusion from the wound surface was collected at 4, 24, 48 h and 5, 7, 14, 21 and 28 days after injury, respectively. The contents of MMP-9 and TGF-beta in the effusion of the wound were measured by zymography and enzyme-linked immunosorbent assay (ELISA), respectively. RESULTS: During the wound healing of blast injury, MMP-9 and TGF-beta exhibited changes that followed a regular pattern, both reaching the peak value at 48 h after the injury. TGF-beta content reached the another peak on day 7. TGF-beta value and MMP-9 contents decreased in the second week after injury and their reduction was no longer parallel. Administration of tissue inhibitor of metalloproteinase (TIMP) in the early phase of injury showed no obvious effect, but during the 2 weeks after the injury, its administration caused decrease in MMP-9 content and increase in TGF-beta content in the effusion. CONCLUSIONS: In the early phase of wound healing, the elevation of MMP-9 and TGF-beta accelerated cell migration to promote the clearance of the inflammatory necrosis tissues, which might be one of the wound healing mechanisms. But overexpression of MMP-9 in the wound may hinder wound healing, and appropriate use of TIMP can accelerate the delayed wound healing.

Distribution of oval cells and c-myc mRNA expression in mouse hepatocarcinogenesis.

BACKGROUND: This study was designed to assess the roles of oval cells and c-myc mRNA in the process of hepatocarcinogenesis and to clarify the function of carcinogene c-myc in the development of hepatocellular carcinoma (HCC) and the mechanism of inhibitory function of uscharidin on HCC in mouse hepatocarcinogenesis. METHODS: A total of 120 clean SD mice were divided into normal group, cancer induction group, and intervention group. The normal group was fed with standard forage while the rest two groups were given p-dimethylaminoazobenzene (DAB) to induce cancer. Thirteen weeks after induction of cancer, the two groups were fed with standard forage and water. Once the pattern was set up, the intervention group was given uscharidin injection into the abdominal cavity from the first week to the 14th week. On the 2nd, 4th, 6th, 8th, 10th, 12th, 14th, 16th, 18th, 20th, 22nd, and 24th week, all mice were killed and biopsied from the liver lobe for pathological analysis. At the same time, the number of tumor nodes was counted and the expression of c-myc mRNA was tested by RT-PCR. RESULTS: Since the 2nd week after cancer induction, proliferated oval cells could be seen in the portal area. Initially, the oval cells appeared in the cortical layer of the portal area, then proliferated gradually and immigrated into the liver parenchyma. In the period of fibrosis after liver proliferation, proliferated heaps of oval cells were noted in both portal and peripheral areas. In the period of carcinomatous change, oval cells could be seen both outside and inside of cancer nodes, but most of them were distributed outside. The c-myc gene was expressed negatively in the liver tissue of mice. The quantity of the expression began to increase at the time of infection of the liver and tended to increase with the degree of hepatic injury. In the period of canceration, the expression level of c-myc mRNA increased gradually. The intervention of uscharidin could not inhibit but delay the increase of the expression of c-myc mRNA. CONCLUSION: Oval cells are closely related to hepatocarcinoma cells, which play an important role in the occurrence and development of hepatocarcinogenesis. Uscharidin can inhibit the occurrence of hepatocarcinogenesis or local spreading at the early stage of cancer induction by DAB, but it cannot inhibit the expression of c-myc.

The expression of c-kit and proliferating cell nuclear antigen in oval cells of rats with hepatocellular carcinoma.

OBJECTIVE: To study the relationship between oval cells and primary hepatocarcinoma and the expression of c-kit and proliferating cell nuclear antigen (PCNA) in oval cells of rats with hepatocellular carcinoma. METHODS: A hundred and twenty clean SD rats were divided into three groups: normal group, cancer-induction group and intervention group. The normal group was fed with standard forage while the rest two groups were fed with 3'-methyl-2-methylamino-azobenzene (DAB) to induce carcinoma for 14 weeks and then fed with standard forage and water. Uscharidin was injected abdominally to the intervention group from the first week to the 14th week. All rats were killed and biopsy specimens were taken from the left and right liver lobes for immunohistochemical staining of c-kit and PCNA on the 2nd, 4th, 6th, 8th, 10th, 12th, 14th, 16th, 18th, 20th, 22nd, and 24th week. RESULTS: From the 2nd to 14th week after liver infection, c-kit positive cells, mainly oval cells were found in the portal area in the carcinoma-induction group and dotted positive pigmentations in liver lobules. In the 22nd week, a large number of cancerous nodes occurred and nuclei heteromorphism was apparent; the number of positive cell decreased but positive cells could be sparsely observed in cancerous nodes. In the 2nd week of the carcinoma-induction process, PCNA positive cells were oval cells in the portal area. In the 4th week, a lot of hepatic cells were positively stained, especially in the central vein area. In the 6th week, PCNA positive cells could be seen in the lobules of the liver. In the 8th week, the number of PCNA cells decreased comparatively. From the 10th to 14th week, oval cells in the portal area were still over-expressed. From the 16th to 24th week, a large number of cancerous nodes occurred and PCNA was over-expressed in some of them. In necrotic cancerous nodes, the para-cancerous PCNA positive cells were sparsely distributed and their number was less than that of PCNA positive cells of cancerous tissues. CONCLUSIONS: Hepatic stem cells originating from the terminal biliary plexus of the portal area are involved in the development of hepatocarcinoma because c-kit positive cells expressed in cancerous nodes, accompany the whole process of the development. In the middle inflammatory period of carcinoma-induction, the expression of PCNA in hepatic cells peaked, but the index decreased in the late inflammatory period and in the proliferated fibrosis stage. The expression of PCNA is a tortuous process, going up, down, then up again from normal tissues to cancerous tissues. Combined with pathological findings, PCNA can be considered as a warning index for carcinomatous cells.