1.Hemorrhage after duodenopancreatectomy
Cai-De LU ; Dan WU ; Feng QIU ; Zhi-Long YAN ; Han-Ting LING ; Ying-Chun SHENG ; Sheng-Dong WU
Chinese Journal of General Surgery 2000;0(12):-
Objective To study the sources and the relationship between the management and the outcome of hemorrhage after cephalic pancreatoduodenectomy.Methods The clinical data of 370 patients who underwent pancreatic resection at the Lihuili Hospital and the Second Affiliated Hospital of Zhejiang University were retrospectively analyzed.Results Postoperative bleeding occurred in 35 patients with 11 deaths.Among those intraabominal bleeding occurred in 14 cases and gastrointestinal hemorrhage occurred in 22,with one case suffering from both.Bleediug developing within 72 hours after operation in 12 cases (early-stage group),which was caused by improper intraoperative homeostasis.In other 23 cases,bleeding 72 hours after operation(later stage group)was caused by the erosion following pancreatic and/or bile leakage.Relaparotomy was performed in 13 cases and endoscopic homeostasis was performed in 3. Relaparotomy or endoscopic homeostasis was superior to that of conservative therapy in the early-stage group (P0.05).Pancreatic or bile leakage was identified as the significant risk factors for the postoperative bleeding.Conclusions In order to prevent the postoperative hemorrhage and to reduce the mortality of pancreatic resection,skillful techniques,expeditious homeostasis,proper management of stump pancreas and the prevention of pancreatic and bile leakage are essential.
2.Effect of Endotoxin on the expression of peroxisome proliferator-activated receptor alpha in the development of nonalcoholic steatohepatitis in rats.
Xia LI ; De Wu HAN ; Long Feng ZHAO ; Lei YIN
Chinese Journal of Hepatology 2005;13(2):89-91
OBJECTIVETo study the effect of endotoxin on the expression of peroxisome proliferator-activated receptor alpha (PPARa) in the development of nonalcoholic steatohepatitis in rats.
METHODSA model of nonalcoholic steatohepatitis (NASH) was developed with Wistar rats fed a chow containing 20% maize oil for 14 weeks. The endotoxin group rats were intraperitoneally injected with lipopolysaccharide (LPS, 1 g/L, 3.0 ml/kg) once 4 hours before the end of the experiment. The concentrations of lipids, endotoxin, tumor necrosis factor-a, malondialdehyde, free fatty acid in plasma and hepatic tissues were determined and the degree of hepatocytic steatosis was studied. The expression of PPARa mRNA in hepatic tissues was measured using reverse transcriptase-polymerase chain reaction (RT-PCR).
RESULTSThe expression of PPARa mRNA in the hepatic tissue of the LPS group was downregulated markedly in comparison to that of the control group. The level of free fatty acid and endotoxin by secreting tumor necrosis factor-a increased and triglyceride accumulated in the liver caused malondialdehyde content to increase, then lipid peroxidation process enhanced and ALT activity increased. Thus, hepatic injury and inflammatory reaction could be accelerated.
CONCLUSIONEndotoxemia can enhance hepatocellular steatosis and lead to NASH due to its downregulating the expression of PPARa mRNA.
Animals ; Down-Regulation ; Endotoxins ; pharmacology ; Fatty Liver ; metabolism ; Liver ; metabolism ; Male ; PPAR alpha ; biosynthesis ; genetics ; RNA, Messenger ; biosynthesis ; genetics ; Random Allocation ; Rats ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction
3.The role of enterogenous endotoxemia in the pathogenesis of non-alcoholic steatohepatitis.
Long-feng ZHAO ; Jun-mei JIA ; De-wu HAN
Chinese Journal of Hepatology 2004;12(10):632-632
Animals
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Endotoxemia
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complications
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Fatty Liver
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etiology
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Hepatitis
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etiology
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Male
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Rats
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Rats, Wistar
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Tumor Necrosis Factor-alpha
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metabolism
4.The effect of intestinal endotoxemia on the balance of Th1/Th2 in patients with hepatitis B.
Hong LI ; De-wu HAN ; Su-mei ZHANG ; Long-feng ZHAO
Chinese Journal of Hepatology 2005;13(12):939-940
Adolescent
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Adult
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Cytokines
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blood
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Endotoxemia
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complications
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Female
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Hepatitis B, Chronic
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complications
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immunology
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Humans
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Male
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Middle Aged
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Th1 Cells
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immunology
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Th2 Cells
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immunology
8.Splenic hamartoma: case report and review of literature.
Hong-bo JIA ; Ying-ping LI ; De-en HAN ; Yao LIU ; Bin ZHANG ; De-quan WU ; Xi CHEN ; Ying JIANG ; Long-xian ZHENG ; Jin-rong DU ; Xue-hai JIANG
Chinese Medical Journal 2006;119(16):1403-1408
Adult
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Female
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Hamartoma
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complications
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diagnosis
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surgery
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Humans
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Kidney Calculi
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complications
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Spleen
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pathology
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surgery
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Splenectomy
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methods
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Splenic Diseases
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complications
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diagnosis
;
surgery
9.Primary diffuse large B-cell lymphoma of the heart: a clinicopathological study.
Zheng-rong WU ; De-sheng WENG ; Yan-qing DING ; Hui-xia HAN ; Mei-gang ZHU
Journal of Southern Medical University 2006;26(10):1481-1483
OBJECTIVETo define the clinicopathological features of primary cardiac large B-cell lymphoma.
METHODA case of primary cardiac large B-cell lymphoma was studied with conventional histopathological and immunohistochemical staining in combination with literature review.
RESULTSThe lesion appeared to originate in the right atrium and involved the venae cavae and the left atrium. Microscopic examination showed diffuse proliferation of large atypical lymphocytes with abundant cytoplasm, vestiealer nuelei, thick nuclear membrane and conspicuous nucleoli. Giant tumor cells scattered in the lesion. The neoplastic cells were positive for CD20 and CD79a.
CONCLUSIONPrimary cardiac lymphoma is extremely rare, and its pathogenesis remains unclear. With non-specific clinical manifestations, the majority of primary cardiac lymphomas are of B-cell lineage and a bad prognosis.
Aged ; Antigens, CD20 ; analysis ; CD79 Antigens ; analysis ; Female ; Heart Neoplasms ; metabolism ; pathology ; Humans ; Lymphoma, Large B-Cell, Diffuse ; metabolism ; pathology
10.The relationship between the peripheral blood of CD61, CD63, PAC-1 and the transplant kidney function.
Yong ZHANG ; De-lin GUAN ; Cheng-qing XIA ; Zhi-you HAN ; Jian-jun XU ; Ju-zhong GAO ; Ke-rang WU
Chinese Journal of Surgery 2003;41(12):881-884
OBJECTIVESTo explore the relationships between the peripheral blood levels of CD61, CD63, PAC-1 and the incidence of acute rejection and tubular necrosis after renal transplantation, and recovery of the graft function.
METHODSThe peripheral blood levels of CD61, CD63, and PAC-1 of 86 patients with uremia in different stages before and after transplantations were analyzed by flow cytometry. The patients were divided into three groups: (1) twenty-nine patients with normal grafts function, (2) hirty with acute rejection and (3) twenty-seven with acute tubular necrosis. The patients with acute rejection were randomly divided into treatment group with anticoagulants and cntrol group.
RESULTSThe peripheral blood levels of CD61, CD63 and PAC-1 significantly increased (P < 0.05) in the patients with acute rejection, in comparison with those with normal grafts function and those with acute tubular necrosis. The peripheral blood levels of CD61, CD63 and PAC-1 in patients with acute rejection in anticoagulants therapy was lower, recovery time of the grafts function was shorter, one-year survival rates of patients and grafts were higher, as compared with those of controls.
CONCLUSIONSThe patients with acute rejection have significantly high peripheral blood levels of CD61, CD63 and PAC-1 before transplantation, however, these values in patients with acute tubular necrosis are not high, this suggesting that acute rejection might relate to platelet activation, while acute tubular necrosis might not relate to it. After anticoagulants therapy in patients with acute rejection, the grafts function might recover faster and their one-year survival rates and grafts might be higher in those with CD61, CD63 and PAC-1 decreasing remarkably.
Adult ; Aged ; Antigens, CD ; blood ; Dual Specificity Phosphatase 2 ; Female ; Graft Rejection ; Humans ; Integrin beta3 ; blood ; Kidney ; physiopathology ; Kidney Transplantation ; Male ; Middle Aged ; Platelet Activation ; Platelet Membrane Glycoproteins ; Protein Phosphatase 2 ; Protein Tyrosine Phosphatases ; blood ; Tetraspanin 30