54 research outputs found

    A Case of Pancreatic Ascites and Pleural Effusion: Confirmation of a Pancreatic Duct Contrast Leakage Using Computed Tomography after Endoscopic Retrograde Cholangiopancreatography

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    A seventy-two year old Japanese man with chronic alcoholism was admitted with increasing epigastric pain and abdominal fullness. He gave a history of bouts of epigastric pain radiating to the back for the past year. At admission, abdominal ultrasonography and computed tomography (CT) demonstrated massive ascites and a pseudocyst in the pancreatic body. A chest X-ray showed bilateral pleural effusion, and the level of amylase was elevated in the serum, urine, ascitic fluid and pleural effusion. First, the patient was treated with nothing by mouth but with intravenous hyperalimentation, however, no improvement was noted after 2 weeks. Then, the patient underwent endoscopic retrograde cholangiopancreatography (ERCP) and abdominal CT after ERCP. They showed irregular dilatation of the pancreatic main duct and branch, and an extravasation of contrast media from the pancreatic duct into the peritoneal cavity, after which the patient underwent surgery. Because no fistula was found during surgery, drainages were retained into the pseudocyst and peritoneal cavity. Due to marked elevation of amylase and protein levels in ascitic fluid and pleural effusion and findings from ERCP and CT after ERCP, pancreatic ascites and pleural effusion was diagnosed. The diagnosis of chronic pancreatitis is due to his history, laboratory data, and irregular dilatation of the pancreatic duct on ERCP. After surgery, his clinical status improved rapidly. We thus described a case of pancreaticoperitoneal fistula demonstrated by CT scan subsequent to ERCP which was treated successfully by surgery

    Development of Large Capacity CO2 Scroll Compressor

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    Wear-Less Technology for Rotary Compressor Using CO2 Refrigerant

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    Suppression of Very Early Stage Of Adipogenesis by Baicalein, a Plant-Derived Flavonoid through Reduced Akt-C/EBPα-GLUT4 Signaling-Mediated Glucose Uptake in 3T3-L1 Adipocytes.

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    Baicalein has been used as a Chinese medicine, and is an abundant plant flavonoid present in fruits and vegetables. Here, we examined the effects of baicalein in adipogenesis and investigated its molecular mechanism in adipocytes. Baicalein lowered the intracellular lipid accumulation and decreased the transcription levels of the adipocyte-specific genes in mouse 3T3-L1 adipocytes. Glucose uptake mediated by glucose transporter 4 (GLUT4) was reduced, causing down-regulation of the intracellular lipid accumulation. These reductions were also observed even when baicalein was added in only early stage of adipogenesis (0-2 days) of 6-day-adipogenesis. Chromatin immunoprecipitation assay showed that baicalein decreased the binding level of C/EBPα protein to the promoter region of the GLUT4 gene. Phosphorylation of Akt at 1 h after the initiation of adipogenesis was inhibited by the treatment with baicalein. Inhibition during only the first 1.5 h after the initiation of adipogenesis by baicalein or an Akt inhibitor was enough to decrease the lipid contents in the cells undergoing adipocyte differentiation for 6 days. These results indicate that baicalein decreased the intracellular lipid accumulation by down-regulation of glucose uptake via repression of Akt-C/EBPα-GLUT4 signaling in the very early stage of adipogenesis of 3T3-L1 adipocytes

    Inhibition of very early stage of adipogenesis in 3T3-L1 cells by baicalein or Akt inhibitor.

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    <p>A, Intracellular triglyceride level. 3T3-L1 cells (undifferentiated cells: U; <i>white column</i>) were differentiated into adipocytes (differentiated cells: D; <i>gray column</i>) for 6 days and treated with baicalein or an Akt inhibitor (Akt Inh.; <i>black columns</i>) for the initial 1.5 h of adipogenesis. Data are presented as the means ± S.D. from three experiments. **<i>p</i><0.01, as indicated by the brackets. B, Expression levels of adipogenic genes. Cells were cultured as described in the legend of Fig 8A. Data are shown as the means ± S.D. from three experiments. **<i>p</i><0.01, as indicated by the brackets. C, ChIP assay. 3T3-L1 cells were cultured as described in the legend of Fig 8A. The results are representative from three experiments. Band intensity was measured with MultiGauge software. D, Change in glucose uptake. 3T3-L1 cells were cultured as described in the legend of Fig 8A. Cells were then incubated with fluorescent 2-NBDG, and then observed under a fluorescence microscope. The results are representative from three experiments. E, Quantification of glucose uptake in baicalein- or Akt inhibitor (Akt Inh.)-treated 3T3-L1 cells. The data are presented as the value relative to that of the undifferentiated cells and are shown as the means ± S.D. from three experiments **<i>p</i><0.01, as indicated by the brackets.</p

    Expression of GLUT4 in baicalein- or Akt inhibitor-treated 3T3-L1 cells.

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    <p>A, Expression of the recombinant mouse GLUT4 protein in 3T3-L1 cells. 3T3-L1 cells were transfected with GLUT4 (pcDNA-mGLUT4) or the empty (pcDNA) vector. GLUT4 levels were detected by Western blot analysis using cell extracts (15 μg/lane). B, Intracellular triglyceride level in GLUT4-transfected cells. 3T3-L1 cells were transfected with GLUT4 vector by electroporation. After 24 h, cells (undifferentiated cells: U; <i>white column</i>) were differentiated into adipocytes (differentiated cells: D; <i>gray column</i>) for 6 days and treated with baicalein or an Akt inhibitor (Akt Inh.; <i>black columns</i>) for the initial 1.5 h of adipogenesis. Data are presented as the means ± S.D. from three experiments. *<i>p</i><0.05, **<i>p</i><0.01, as indicated by the brackets. C, Change in glucose uptake in GLUT4-transfected cells. 3T3-L1 cells were cultured as described in the legend of Fig 9B. Cells were then incubated with fluorescent 2-NBDG, and then observed under a fluorescence microscope. The results are representative from three experiments. D, Measurement of glucose uptake in GLUT4-transfected cells. Data are presented as the value relative to that of the undifferentiated cells and are shown as the means ± S.D. from three experiments **<i>p</i><0.01, as indicated by the brackets.</p
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