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Objective To investigate the value of virtual touch tissue imaging (VTI) in the differential diagnosis of small solid thyroid nodules.Methods 35 patients with 41 small thyroid nodules were examined by conventional ultrasound and VTI examination.The stiffness of the nodules in VTI images was scored.Area ratios of VTI and gray scale images of nodules were calculated.The pathological diagnosis was used as the gold standard.The ROC curve was drawn to determine the cut off point of area ratio to predict thyroid cancer.Results 41 small thyroid nodules were confirmed by pathological diagnosis,including 23 benign and 18 malignant nodules.Compared with benign nodules,the ratio of VTI hardness score ≥4 was significantly higher in the malignant nodules (88.9％ vs 8.7％,P ＜0.01).Compared with benign nodules,the area ratios of malignant nodules were higher (1.67 ± 0.16 vs 1.23 ± 0.12,P ＜0.01).When 1.46 was set as the cut off point of areas ratio,the sensitivity and specificity of diagnosing thyroid cancer were 88.9％ and 95.7％,respectively.Conclusions VTI can provide information about thyroid nodules hardness.It has high value in the differential diagnosis of small solid thyroid nodules.
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<p><b>OBJECTIVE</b>To investigate the effect of lovastatin on proliferation and extracellular matrix secretion of hepatic stellate cells in vitro.</p><p><b>METHODS</b>Rat hepatic stellate cells were incubated with different concentration of lovastatin and geranyl geranypyrophosphate. Cell proliferation was assessed by MTT colorimetric assay. Cell cycle was analysed by flow cytometry. Type IV collagen and laminin were determined by ELISA, and c-jun and c-fos expression by immunocytochemistry and computer video text analysis system.</p><p><b>RESULTS</b>Addition of 0.1 to 50 micromol/L lovastatin into culture medium had no toxicity to hepatic stellate cells, but could significantly inhibit hepatic stellate cell proliferation and provoke G0/G1 phase arrest in dose-dependent manner, and could also markedly inhibit the c-jun and c-fos expression and type IV collagen and laminin secretion, which could partly be antagonized by geranyl geranypyrophosphate.</p><p><b>CONCLUSIONS</b>Lovastatin can significantly inhibit hepatic stellate cell proliferation and type IV collagen and laminin secretion, which might be partly related to its inhibitory effect on geranyl geranypyrophosphate formation.</p>
Subject(s)
Animals , Rats , Cell Cycle , Cell Division , Cell Proliferation , Cells, Cultured , Collagen Type IV , Extracellular Matrix , Bodily Secretions , Hepatic Stellate Cells , Bodily Secretions , Lovastatin , PharmacologyABSTRACT
Objective: To study the effect of intracellular-free calcium and the expression of Fas and Fas L on the process of pancreatic carcinoma cell apoptosis. Methods: Apoptosis induced by 2 μmol/L arsenic trioxide in pancreatic cancer cell lines SW-1990 was investigated.Concentration of intracellular-free calcium （［Ca2+］i） was determined by Fura-2a fluorescein load technique. Fas and FasL were determined by flow cytometry. Results: Pancreatic cancer cells treated with 2 μmol/L arsenic trioxide presented apoptotic features: intact cell membrane, chromatin condensation, nucleic fragmentation and apoptotic body formation; agarose electrophoresis showed marked ladder; flow cytometery analysis showed a sub-G1 cell peak. In the process of pancreatic carcinoma cell apoptosis Fas and FasL and the ［Ca2+］i were significantly higher than that in the control. Conclusion: The pancreatic cancer cell apoptosis induced by arsenic trioxide is related to Fas and FasL expression by the cancer cells and the ［Ca2+］i increase in the cancer cells.
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Objective: To select the telomerase positive cancer cell lines of gastrointestinal tract and to provide a convinced methodology for future telomerase study. Methods: Fifteen cancer cell lines (carcinoma of stomach 4, of liver 6, of pancreas 2, of colon 3) were cultured and telomerase activity were detected by TRAP-ELISA. The normal hepatic cells were taken as control. Results: Thirteen cell lines were telomerase positive in the 15 lines(86.7%). Conclusion: Most of gastrointestinal tract cancer lines express telomerase, indicating the detection of telomerase activity has clinical potential.
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Objective To investigate the effect of recombinant human tumor necrosis factor (rhTNF) on telomerase activity in hepatoma cell line HepG2 cells and HepG1 6 cells. Methods TRAP ELISA method was used to determine the telomerase activity in HepG2 and HepG1 6 cells which were treated by different concentrations of rhTNF; plasmid which had been inserted 800 bp of the hTERT promoter was transiently transfected into HepG2 cells by Lipofect, and different concentrations of rhTNF were added into culture media 2 hours later, then the activity of the hTERT promoter was tested 48 hours after transfection. Results The telomerase activity of HepG2 was suppressed by rhTNF in a dose dependent manner. The expression of hTERT promoter was inhibited linearly with the dose of rhTNF within the range of 10～1 000 IU/ml. Conclusions Above results suggest that the anti tumor activity of rhTNF may attribute to its inhibitory effect on hTERT promoter expression.
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Objective To investigate the effect of taurine on proliferation / apoptosis of rat hepatic stellate cells in culture and the possible mechanism involved. Methods Rat hepatic stellate cells were incubated with different concentration of taurine. Cell proliferation was assessed by MTT colorimetric assay, cell cycle and apoptosis were analysed by flow cytometry, apoptotic morphology was examined by vital staining of acridine orange, c-jun and c-fos expression was determined by immunocytochemistry and computer video text analysis system. Results Administration of 5-50 mmol/L taurine into culture medium had no toxicity to hepatic stellate cells, but could significantly inhibit hepatic stellate cell proliferation in dose-dependent manner, increase the number of cell in G 0/G 1 phase and decrease the numbers in S phase. Taurine could also markedly inhibit c-jun and c-fos expressions ( P
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AIM: To observe the dynamic changes of plasma levels of nitric oxide(NO) and endothelin (ET-1) in portal veins of the rats during prehepatic portal hypertension, and investigate the role of them in hyperdynamic circulation. METHODS: The models of prehepatic portal hypertension were established in Sprague-Dawley rats by means of partial portal vein ligation (PVL). The plasma levels of nitrite/nitrate (NO - 2/NO - 3) and ET-1 in the portal veins were detected by the method of nitric reductase and radioimmunoassay, respectively. In this study, rats were divided into normal, sham operation (SO) and PVL group. SO and PVL rats were divided into several subgroups according to different time after operations. Meanwhile, the changes of several hemodynamic indexes in these rats were also measured. RESULTS: The levels of NO - 2/NO - 3 were significantly increased and ET-1 were significantly decreased in rats at different time after PVL compared with normal control, whereas the hemodynamic indexes changed accordingly. CONCLUSION: The portal hypertensive rats are in hyperdynamic circulatory state (HCS). NO and ET-1 may play an important role in the induction and maintenance of HCS.
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Objective: To study the effect of intracellular free calcium and the expression of Fas and Fas L on the process of pancreatic carcinoma cell apoptosis. Methods: Apoptosis induced by 2 ?mol/L arsenic trioxide in pancreatic cancer cell lines SW 1990 was investigated.Concentration of intracellular free calcium ([Ca 2+ ]i) was determined by Fura 2a fluorescein load technique. Fas and FasL were determined by flow cytometry. Results: Pancreatic cancer cells treated with 2 ?mol/L arsenic trioxide presented apoptotic features: intact cell membrane, chromatin condensation, nucleic fragmentation and apoptotic body formation; agarose electrophoresis showed marked ladder; flow cytometery analysis showed a sub G 1 cell peak. In the process of pancreatic carcinoma cell apoptosis Fas and FasL and the [Ca 2+ ]i were significantly higher than that in the control. Conclusion: The pancreatic cancer cell apoptosis induced by arsenic trioxide is related to Fas and FasL expression by the cancer cells and the [Ca 2+ ]i increase in the cancer cells.