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.

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

Adolescent ; Adult ; Cytokines ; blood ; Endotoxemia ; complications ; Female ; Hepatitis B, Chronic ; complications ; immunology ; Humans ; Male ; Middle Aged ; Th1 Cells ; immunology ; Th2 Cells ; immunology

Animals ; Endotoxemia ; complications ; Fatty Liver ; etiology ; Hepatitis ; etiology ; Male ; Rats ; Rats, Wistar ; Tumor Necrosis Factor-alpha ; metabolism

Endotoxemia ; metabolism ; pathology ; HMGB1 Protein ; Humans ; Liver ; metabolism ; pathology

Endotoxins ; Humans ; Insulin-Like Growth Factor Binding Proteins ; Liver Cirrhosis

Adult ; Female ; Hamartoma ; complications ; diagnosis ; surgery ; Humans ; Kidney Calculi ; complications ; Spleen ; pathology ; surgery ; Splenectomy ; methods ; Splenic Diseases ; complications ; diagnosis ; surgery

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

OBJECTIVETo study the potential role of mast cells and the related molecular mechanism in chronic hepatitis (CH) using a rat model system.

METHODSThirty Wistar rats (15 males, 15 females; weight range: 230-290 g) were randomly divided into the normal contrast (NC) group and experimental CH group. The CH group received subcutaneous injection of CCl4 and a diet high in cholesterol and alcohol content and low in protein and choline content. Throughout the 4-week modeling period, aseptic blood samples were taken to test plasma tryptase (TS) and hyaluronic acid (HA) levels. The rats were euthanized to assess the changes in liver mast cells by histology and morphology analyses and the changes in liver expression of c-kit and stem cell factor (SCF) proteins by immunohistochemistry and mRNAs by RT-PCR.

RESULTSCompared to the NC group, the CH group had higher plasma and liver concentration of HA (78.09 +/- 38.55 vs. 145.14 +/- 52.54 ng/ml, 51.58 +/- 20.45 vs. 106.59 +/- 43.15 ng/100 mg; t = 2.457 and 2.825 respectively, both P less than 0.05) and TS (0.416 +/- 0.143 vs 0.753 +/- 0.210 mg/ml; t = 4.165, P less than 0.05). The CH group also showed fatty degeneration and fibrosis with many degranulating and degranulated mast cells filled with purple granula located around the liver blood vessels and in fiber-intervals. The CH livers also showed a significantly higher number of mast cells (2.167 +/- 0.924 vs. NC: 10.92 +/- 1.575; t = 7.633, P less than 0.05) and stronger intensity of c-kit staining (2.783 +/- 0.577 vs. 12.86 +/- 3.126; t = 9.511, P less than 0.05) and SCF staining (3.383 +/- 1.583 vs. 15.58 +/- 6.431; t = 9.625, P less than 0.05). The expressions of c-kit and SCF were positively correlated with HA level (r = 0.478 and 0.556 respectively, both P less than 0.05). The c-kit and SCF mRNA expression levels were also significantly higher in the CH liver tissues.

CONCLUSIONMast cell degranulation and histamine release is significantly increased under conditions of chronic hepatitis, and the related mechanism may involve up-regulation of the membrane receptor c-kit and its ligand SCF.

Animals ; Cell Degranulation ; Disease Models, Animal ; Female ; Hepatitis, Chronic ; metabolism ; pathology ; Hepatocytes ; metabolism ; Liver ; metabolism ; Liver Cirrhosis ; metabolism ; pathology ; Male ; Mast Cells ; metabolism ; physiology ; Proto-Oncogene Proteins c-kit ; metabolism ; RNA, Messenger ; genetics ; Rats ; Rats, Wistar ; Stem Cell Factor ; metabolism