Publications by authors named "Chad A Wiesenauer"

Purpose: The spectrum of pediatric biliary tract disease is changing. The goal of this study was to examine the causes and comorbidities of pediatric gallbladder disease at our institution.

Methods: We performed a retrospective chart review on consecutive patient at Kosair Children's Hospital who underwent cholecystectomy over a 9-year time period ending in 2012.

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Background: Patients with ulcerative colitis (UC) often report dietary intolerances. Our aim was to assess the effects of proctocolectomy (PC) for UC on dietary intolerances.

Methods: A novel disease-specific questionnaire was used.

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The MEK-ERK growth signaling pathway is important in human hepatocellular carcinoma (HCC). To evaluate the targeting of this pathway in HCC, we characterized a novel, orally-active MEK inhibitor, PD184161, using human HCC cells (HepG2, Hep3B, PLC, and SKHep) and in vivo human tumor xenografts. PD184161 inhibited MEK activity (IC50 = 10-100 nM) in a time- and concentration-dependent manner more effectively than PD098059 or U0126.

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Hypothesis: Pancreaticoduodenectomy (PD) is a safe procedure for a variety of periampullary conditions.

Design: Retrospective review of a prospectively collected database.

Setting: Academic tertiary care hospital.

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Background: Human hepatocellular carcinoma (HCC) is associated with increased expression and activity of mitogen-activated protein kinase (MAPK) signaling intermediates (ie, MEK, ERK).

Study Design: We determined the effects of MEK-ERK signaling on proliferation, cell cycle, apoptosis, and tumorigenicity of HCC in vitro. HCC cell lines were treated with MEK enzyme-specific inhibitors, PD098059 and U0126, and ERK1,2 oligonucleotide antisense.

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Hypothesis: Malignant intraductal papillary mucinous neoplasms (IPMNs) can be predicted before surgery.

Design: Retrospective review of a prospectively collected database.

Setting: Academic, urban, tertiary care hospital.

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Nonsteroidal anti-inflammatory drugs (NSAIDs) may be effective treatment for pancreatic cancer. We have previously demonstrated that NSAIDs suppress pancreatic cell growth in vitro by inhibiting cell cycle progression but have little effect on apoptosis. In fact, we have shown that NSAIDs, in some instances, increase Akt phosphorylation in human pancreatic carcinoma cells suggesting activation of the phosphatidylinositol 3'-kinase (PI3K)-Akt survival (antiapoptotic) pathway.

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