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Articles by T. D Nguyen
Total Records ( 2 ) for T. D Nguyen
  M Yamamoto , M. S Hayashi , N. T Nguyen , T. D Nguyen , S McCloud and D. K. Imagawa

Objective  To investigate the use of Seamguard, a bioabsorbable staple line–reinforcement product, to prevent pancreatic leak after distal pancreatectomy.

Design, Setting, and Participants  A retrospective study examined 85 consecutive patients undergoing distal pancreatectomy at an academic institution from September 5, 1997, to September 30, 2007.

Main Outcome Measures  Pancreatic fistula and overall mortality and morbidity.

Results  In February 2004, the use of Seamguard in distal pancreas resections was introduced at our institution. Indications for resection included trauma (11 patients), neoplasms (62 patients), and chronic pancreatitis (12 patients). Pancreatic leak was defined as drain output of 25 mL/d or more 7 days postoperatively with a drain amylase level of 1000 U/L or more. Pancreatic leak occurred in 10 of 38 patients (26%) undergoing conventional resection with suture ligation of the pancreatic duct or nonreinforced stapled resection vs 2 of 47 patients (4%) undergoing staple resection using Seamguard reinforcement. Multivariate analysis showed that use of Seamguard with the stapler independently decreased the risk for pancreatic fistula after distal pancreatectomy (odds ratio, 0.07; 95% confidence interval, 0.01-0.43; P = .01).

Conclusions  The use of Seamguard is quickly becoming a common adjunct in distal pancreas resections. Our study shows a lower incidence of pancreatic leak after distal pancreatectomy with the use of this staple line–reinforcing product.

  S. R Jung , B Hille , T. D Nguyen and D. S. Koh

Exocytosis is evoked by intracellular signals, including Ca2+ and protein kinases. We determined how such signals interact to promote exocytosis in exocrine pancreatic duct epithelial cells (PDECs). Exocytosis, detected using carbon-fiber microamperometry, was stimulated by [Ca2+]i increases induced either through Ca2+ influx using ionomycin or by activation of P2Y2 or protease-activated receptor 2 receptors. In each case, the exocytosis was strongly potentiated when cyclic AMP (cAMP) was elevated either by activating adenylyl cyclase with forskolin or by activating the endogenous vasoactive intestinal peptide receptor. This potentiation was completely inhibited by H-89 and partially blocked by Rp-8-Br-cAMPS, inhibitors of protein kinase A. Optical monitoring of fluorescently labeled secretory granules showed slow migration toward the plasma membrane during Ca2+ elevations. Neither this Ca2+-dependent granule movement nor the number of granules found near the plasma membrane were detectably changed by raising cAMP, suggesting that cAMP potentiates Ca2+-dependent exocytosis at a later stage. A kinetic model was made of the exocytosis stimulated by UTP, trypsin, and Ca2+ ionophores with and without cAMP increase. In the model, without a cAMP rise, receptor activation stimulates exocytosis both by Ca2+ elevation and by the action of another messenger(s). With cAMP elevation the docking/priming step for secretory granules was accelerated, augmenting the releasable granule pool size, and the Ca2+ sensitivity of the final fusion step was increased, augmenting the rate of exocytosis. Presumably both cAMP actions require cAMP-dependent phosphorylation of target proteins. cAMP-dependent potentiation of Ca2+-induced exocytosis has physiological implications for mucin secretion and, possibly, for membrane protein insertion in the pancreatic duct. In addition, mechanisms underlying this potentiation of slow exocytosis may also exist in other cell systems.

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