Objective To assess three-dimensional color Doppler energy (3D-CDE) in the diagnosis of liver tumors.Methods Vascular pattern of 2D- and 3D-CDE were used to analyze 106 tumors of 96 patients,and their sensitivity and specify were calculated respectively.Three-dimensional volumetric measurement was used to calculate the volume,vessel counts of tumor,as well as the ratio of vessel counts and volume,whereas vascular index (VI) of both benign and malignant lesions were assessed.Results ①Using the vascular pattern of IE as diagnosis standard of liver malignant,the sensitivity and specificity of 2D-CDE and 3D-CDE were 21.33%,100% and 81.33%,100%,respectively) using the vascular pattern of II and Ⅲ,the sensitivity and specificity were 73.33%,67.74% and 100%,45.16%,respectively.②Mean VI was 0.38 counts/cm~3 of malignant tumors and 0.18 counts/cm~3 of 31 benign tumors (P<0.05),The sensitivity and specificity in diagnosing malignant tumors of liver was 78.67% and 87.10%,respectively with VI>0.30 counts/cm~3.Conclusion The vascular pattern of 3D-CDE HI and VI>0.30 counts/cm~3 may be taken as parameters for the diagnosis of malignant liver tumor.

ObjectiveTo evaluate the changes of Ag-NORs in patients with gallbladder carcinoma.MethodsAg-NORs in the peripheral blood lymphocytes,bile lymphocytes and the mucosa of gallbladder were detected by a cell image analysis of KL-2 in 20 normal volunteers,90 cholecystitis cases, and 20 gallbladder carcinomas. ResultsAg-NORs in peripheral blood lymphocytes (PBL) and bile lymphocytes (BL) in cholecystitis were lower than that in normal group(P

Objective To investigate the changes of tumor necrosis factor-?(TNF-?) and platelet-derived growth factor(PDGF) in gallbladder carcinoma (GA) patients with cell wall-deficient bacleria(L-form) infection .Methods The levels of TNF-? in gallbladder mucosa were detected by radioimmunoassay and the activity of PDGF was detected by bioactivity assay in patients with GA or cholecystitis and normal gallbladder(control group).Results The positive detection rates of L-forms in gallbladder mucosa of gallbladder carcinoma , chronic cholecystitis, and control group were 80.0%(16/20),82.5%(33/40) and 0(0/20), respectively.The TNF-? and PDGF levels in patients with L-form infection-positive gallbladder carcinoma were significantly higher than those in patients without L-form infection and in control group.The levels of TNF-a and PDGF in patients with L-form infection positive chronic cholecystitis were significantly higher than those in patients without L-form infection and in control group.Conclusions L-form may be one of the direct factors leading to the increase in PDGF during gallbladder oncogenesis,and there is positive correlation between PDGF and gallbladder oncogenesis when L-form induces inflammatory reaction and predisposes gallbladder mucosa to develope neoplasms.

[ABSTRACT]AIM:ToinvestigatetheeffectofD4F,anapolipoproteinA-Imimeticpeptide,onoxidizedlow-density lipoprotein ( ox-LDL)-induced macrophage apoptosis and activation of caspase-12, a key molecule in endoplasmic reticulum stress ( ERS )-associated apoptotic pathway, and to elucidate the underlying molecular mechanisms. METHODS:RAW264.7 macrophages were pretreated with D4F (12.5, 25 and 50 mg/L), 4-phenylbutyric acid (PBA, 5 mmol/L) or diphenyleneiodonium ( DPI, 5 μmol/L) for 1 h and then treated with ox-LDL (100 mg/L) or tunicamycin ( TM, 4 mg/L) for 24 h.The cell viability and apoptosis were determined by MTT assay and TUNEL detection, respective-ly.The levels of malondialdehyde ( MDA) and reactive oxygen species ( ROS) in the cells and the activities of superoxide dismutase ( SOD) and nicotinamide adenine dinucleotide phosphate ( NADPH) oxidase were determined.The protein level of caspase-12 was examined by Western blot analysis.RESULTS: Similar to the ERS inhibitor PBA, D4F protected RAW264.7 macrophages from ox-LDL or TM ( an ERS inducer)-induced decrease in the viability and increase in apoptotic rate in a dose-dependent manner.Like DPI (an oxidative stress inhibitor), D4F significantly inhibited ox-LDL-induced ox-idative stress, as expressed by the decreased generation of ROS and MDA ( P<0.01) , the increased activity of SOD and the decreased activity of NADPH oxidase (P<0.05).Moreover, similar to PBA and DPI, D4F significantly suppressed ox-LDL-induced activation of caspase-12 in a concentration-dependent manner ( P<0.05) .Furthermore, D4F also inhibi-ted the caspase-12 activation induced by TM (P<0.05).CONCLUSION: D4F inhibits macrophage apoptosis induced by ox-LDL, and the mechanism is at least partially by reducing oxidative stress and inhibiting the activation of caspase-12.