Cholecystectomy, Laparoscopic ; methods ; Cholelithiasis ; surgery ; Female ; Humans ; Middle Aged ; Situs Inversus ; complications

OBJECTIVETo analyze the cause of abdominal hemorrhage after reduce-size liver transplantation in rats.

METHODSHealthy female SD rats were used as the donors and male SD rats as the recipients (weighing 260-280 g), with the recipients weighing 10 g more than that of the donors. The donor operation was performed by the same surgeon under direct vision, and the liver graft size reduction procedure was completed in the donor operation. The recipient operation was performed by two surgeons under direct vision.

RESULTSA total of 270 SD rats received reduce-size liver transplantation successfully, and 44 of the rats died from intra-abdominal hemorrhage. The abdominal hemorrhages, listed in the order of incidences, included anastomotic hemorrhage of the inferior vena cava of the superior liver (28 cases), subcapsular hemorrhage of the liver (9 cases), ligation hemorrhage of the left outboard lobe, the nipple lobe and the triangle lobe of the liver (9 , 7 and 7 cases, respectively), hemorrhage of the right suprarenal vein and lumbar veins (5 cases), hemorrhage of the mechanical injury (4 cases), cuff hemorrhage of the portal vein and inferior vein cava of the inferior liver (both 4 cases). Eight rats had anastomotic hemorrhage of the inferior vena cava of the superior liver and ligation hemorrhage of the left outboard lobe, 5 had hemorrhage of the two ligation points of the reduce-size liver; for management of the hemorrhage, 10 rats received suture or/and ligature, and 6 had washing and hot water bath.

CONCLUSIONThe most common cause of hemorrhage after reduce-size liver transplantation in rats is the anastomotic hemorrhage of the inferior vena cava of the superior liver, and this finding may provide clues for improving the success rate of reduced size liver transplantation in rats.

Abdominal Cavity ; Animals ; Female ; Liver Regeneration ; Liver Transplantation ; adverse effects ; methods ; Male ; Organ Size ; Postoperative Hemorrhage ; etiology ; Rats ; Rats, Sprague-Dawley

BACKGROUND: With the popularity of laparoscopic cholecystectomy, common bile duct injury has been reported more frequently. There is no perfect method for repairing porcine biliary segmental defects.METHODS: After the decellularization of human arterial blood vessels, the cells were cultured with GFP⁺ (carry green fluorescent protein) porcine bile duct epithelial cells. The growth and proliferation of porcine bile duct epithelial cells on the human acellular arterial matrix (HAAM) were observed by hematoxylin-eosin (HE) staining, electron microscopy, and immunofluorescence. Then, the recellularized human acellular arterial matrix (RHAAM) was used to repair biliary segmental defects in the pig. The feasibility of it was detected by magnetic resonance cholangiopancreatography, liver function and blood routine changes, HE staining, immunofluorescence, real-time quantitative PCR (RT-qPCR), and western blot.RESULTS: After 4 weeks (w) of co-culture of HAAM and GFP? porcine bile duct epithelial cells, GFP⁺ porcine bile duct epithelial cells grew stably, proliferated, and fused on HAAM. Bile was successfully drained into the duodenum without bile leakage or biliary obstruction. Immunofluorescence detection showed that GFP-positive bile duct cells could still be detected after GFP-containing bile duct cells were implanted into the acellular arterial matrix for 8 w. The implanted bile duct cells can successfully resist bile invasion and protect the acellular arterial matrix until the newborn bile duct is formed.CONCLUSION: The RHAAM can be used to repair biliary segmental defects in pigs, which provides a new idea for the clinical treatment of common bile duct injury.
Bile ; Bile Ducts ; Blood Vessels ; Blotting, Western ; Cholangiopancreatography, Magnetic Resonance ; Cholecystectomy, Laparoscopic ; Coculture Techniques ; Common Bile Duct ; Duodenum ; Epithelial Cells ; Fluorescent Antibody Technique ; Humans ; Infant, Newborn ; Liver ; Methods ; Microscopy, Electron ; Polymerase Chain Reaction ; Swine ; Tissue Engineering

Objective: To investigate the expression of myocyte enhancer factor 2B (MEF2B) in mantle cell lymphomas (MCL), and to analyze the correlation between the expression of MEF2B and pathological subtypes, structural subtypes, SOX11 expression and its clinical significance. Methods: Paraffin-embedded tissues were stained with HE, immunohistochemistry (EnVision method) and fluorescence in situ hybridization (FISH) , in addition, the clinical and pathological data of 60 cases of MCL were collected at Sun Yat-sen University Foshan Hospital and Sun Yat-sen University Cancer Center from January,2002 to May, 2019 for analysis. Results: Of the 60 MCLs, males is predominant (M∶F=3∶1). Histologically, the typical MCL is the majority (classical MCL: variant type MCL=48 cases:12 cases) . Fifty cases were classified into non-complete FDC meshwork type MCL, and the remaining 10 cases were classified into the complete-FDC meshwork type MCL group. Patients with classical MCL were more than 60 years old. The coexistent lesion sites both node and extranode in pathological subtype or structural subtype was the most common lesion sites. SOX11(+) MCL was common in classical MCL (P=0.040) and tended to be complete-FDC meshwork type MCL (P=0.086). The expression rate of MEF2B in MCL was 60.0%(36/60). This rate of MEF2B in classical type, complete-FDC meshwork type and SOX11(+) MCL was significantly higher than that variant type, no complete-FDC meshwork type, SOX11(-)MCL (P<0.05), respectively. There was no difference in clinical characteristics of MCL between MEF2B positive and negative groups. Compared with SOX11(-)MCL, the percentage of MEF2B expressed in tumor cells of SOX11(+)MCL was significantly higher (P=0.027). The expression of MEF2B was not related to the proliferation of tumor cells (P=0.341). There was no significant difference in the survival rate between different expression groups of MEF2B and SOX11 (P=0.304 and P=0.819, respectively). Only the mortality of variant type (blastoid/pleomorphic) MCL within 2 years was significantly higher than that of classical type MCL (P<0.05). Conclusions The expression of MEF2B in MCL is related to the pathological subtypes, structural subtypes and the expression of SOX11, but not to the proliferation and prognosis. The high mortality rate within 2 years is only found in variant MCL. However, the role of MEF2B in MCL needs to be further studied.