Clinical characteristics and prognostic risk factors of candidemia in non-neutropenic patients: a retrospective cohort study.

This study aimed to determine the clinical characteristics and the prognostic risk factors in non-neutropenic patients with candidemia. Data were retrospectively collected through the medical record information system. Non-neutropenic patients with candidemia were relatively aged, with a more than one-third rate of in-hospitalization mortality.

Cyclooxygenase-2 induces angiogenesis in pancreatic cancer mediated by prostaglandin E.

The purpose of the present study was to elucidate the effects of cyclooxygenase 2 (COX-2) on the expression of vascular endothelial growth factor (VEGF) and prostaglandin E (PGE) in pancreatic cancer and , and to clarify the potential mechanism of COX-2-induced angiogenesis of pancreatic cancer. The study analysis was conducted in the pancreatic cancer PC-3 cell line. The expression of COX-2 and VEGF in human pancreatic cancer tissue was analyzed by immunohistochemistry.

Downregulation of GEP100 Improved the Growth Inhibition Effect of Erlotinib Through Modulating Mesenchymal Epithelial Transition Process in Pancreatic Cancer.

Objective: The epidermal growth factor receptor is overexpressed in the majority of pancreatic cancer. Epidermal growth factor receptor tyrosine kinase inhibitor erlotinib was approved to treat patients combining with gemcitabine. However, the sensitivity is low.

Multiple Lymphomatous Polyposis of the Intestine with Ileocecal Intussusception Due to Mantle Cell Lymphoma: A Case Report of a 34-Year-Old Man.

BACKGROUND Multiple lymphomatous polyposis of the gastrointestinal tract can be associated with the B-cell lymphoma variant, mantle cell lymphoma, with most cases having been described in patients who are more than 50 years-of-age. A rare case of multiple lymphomatous polyposis due to mantle cell lymphoma is reported in a 34-year-old man. CASE REPORT A 34-year-old man presented with paroxysmal abdominal pain followed by spontaneous remission, which had been previously diagnosed as gastritis.

microRNA-1228 impairs the pro-angiogenic activity of gastric cancer cells by targeting macrophage migration inhibitory factor.

Our previous study has shown that microRNA-1228 (miR-1228) is downregulated in gastric cancer tissues and restoration of its expression retards tumor growth in a gastric cancer xenograft model. In this work, we aimed to explore the role of miR-1228 in gastric cancer cell cycle progression and angiogenesis and to identify its functional target gene(s). It was found that miR-1228 overexpression significantly inhibited the proliferation and colony formation of gastric cancer cells, compared to vector-transfected cells.

Sonic Hedgehog-GLI Family Zinc Finger 1 Signaling Pathway Promotes the Growth and Migration of Pancreatic Cancer Cells by Regulating the Transcription of Eukaryotic Translation Initiation Factor 5A2.

Objectives: The Hh (hedgehog) signaling pathway is still waiting for further studies because its downstream molecular mechanism remains elusive. Because EIF5A2 (eukaryotic translation initiation factor 5A2) gene was up-regulated upon Gli1 (GLI family zinc finger 1) in pancreatic cancer (PC) cells, we speculated that this pathway might promote tumor progression through regulating EIF5A2.

Methods: We investigated regulation effect of Hh signaling pathway to EIF5A2 gene transcription by Gli1 knockdown or overexpression in PC cell lines first.

Loss of Activin Receptor Type 1B Accelerates Development of Intraductal Papillary Mucinous Neoplasms in Mice With Activated KRAS.

Background & Aims: Activin, a member of the transforming growth factor-β (TGFB) family, might be involved in pancreatic tumorigenesis, similar to other members of the TGFB family. Human pancreatic ductal adenocarcinomas contain somatic mutations in the activin A receptor type IB (ACVR1B) gene, indicating that ACVR1B could be a suppressor of pancreatic tumorigenesis.

Methods: We disrupted Acvr1b specifically in pancreata of mice (Acvr1b(flox/flox);Pdx1-Cre mice) and crossed them with LSL-KRAS(G12D) mice, which express an activated form of KRAS and develop spontaneous pancreatic tumors.

Smad4 loss synergizes with TGFα overexpression in promoting pancreatic metaplasia, PanIN development, and fibrosis.

Aims: While overexpression of TGFα has been reported in human pancreatic ductal adenocarcinoma (PDAC), mice with overexpressed TGFα develop premalignant pancreatic acinar-to-ductal metaplasia (ADM) but not PDAC. TGF-β signaling pathway is pivotal to the development of PDAC and tissue fibrosis. Here we sought to investigate the interplay between TGFα and TGF-β signaling in pancreatic tumorigenesis and fibrosis, namely via Smad4 inactivation.

Sonic hedgehog-Gli1 signaling pathway regulates the epithelial mesenchymal transition (EMT) by mediating a new target gene, S100A4, in pancreatic cancer cells.

Aims: The hedgehog signaling pathway plays an important role in EMT of pancreatic cancer cells, but the precise mechanisms remain elusive. Because S100A4 as a key EMT moleculer marker was found to be upregulated upon Gli1 in pancreatic cancer cells, we focused on the relationship between Shh-Gli1 signals and S100 genes family.

Methods: On the base of cDNA microarray data, we investigated regulating mechanism of Gli1 to some members of S100A genes family in pancreatic cancer cell lines firstly.

Restoration of miR-1228* expression suppresses epithelial-mesenchymal transition in gastric cancer.

Dysregulated miRNAs play critical roles during carcinogenesis and cancer progression. In the present study, the function of miR-1228* in regulating cancer progression was investigated in gastric cancer. Decreased expression of miR-1228* was observed in human gastric cancer tissues comparing to normal tissues.

Genome-wide screening reveals an EMT molecular network mediated by Sonic hedgehog-Gli1 signaling in pancreatic cancer cells.

Aims: The role of sonic hedgehog (SHH) in epithelial mesenchymal transition (EMT) of pancreatic cancer (PC) is known, however, its mechanism is unclear. Because SHH promotes tumor development predominantly through Gli1, we sought to understand its mechanism by identifying Gli1 targets in pancreatic cancer cells.

Methods: First, we investigated invasion, migration, and EMT in PC cells transfected with lentiviral Gli1 interference vectors or SHH over-expression vectors in vitro and in vivo.

Down-regulation of GEP100 causes increase in E-cadherin levels and inhibits pancreatic cancer cell invasion.

Aims: Invasion and metastasis are major reasons for pancreatic cancer death and identifying signaling molecules that are specifically used in tumor invasion is of great significance. The purpose of this study was to elucidate the role of GEP100 in pancreatic cancer cell invasion and metastasis and the corresponding molecular mechanism.

Methods: Stable cell lines with GEP100 knocked-down were established by transfecting GEP100 shRNA vector into PaTu8988 cells and selected by puromycin.

[Effect of metoclopramide on capsule endoscopy examination: a randomized study].

Objective: To investigate the effect of metoclopramide on capsule endoscopy (CE) examination.

Methods: Total 116 patients referred for CE were randomized into two groups with 58 patients in each group. In treatment group patients received 10 mg metoclopramide intramuscular injection after swallowing the capsule and in control group no metoclopramide was administered.

K-Ras resides on the Arf6-mediated CIE system and its active type interacted with Arf6T27N.

Ras is known as an oncogene transferring signals from the plasma membrane. Recent studies have demonstrated that plasma membrane was not the unique platform for Ras signaling. Ras could also be endocytosed and transported to different endomembrane compartments, evoking different signal pathways there.

ADP-ribosylation factor like 7 (ARL7) interacts with alpha-tubulin and modulates intracellular vesicular transport.

ADP-ribosylation factor (ARF) like 7 (ARL7, also named ARL4C) is a member of ARL family and recent studies showed that it is involved in the AI-dependent cholesterol secretion process. Yet its biological function remains largely unknown. Using a MALDI-TOF/MS analysis, we identified alpha-tubulin interacted with ARL7.

Selective inhibition of cyclooxygenase-2 suppresses the growth of pancreatic cancer cells in vitro and in vivo.

Cyclooxygenase-2 (COX-2), a prostaglandin synthetase, is involved in development of certain tumors. We therefore analyzed COX-2 expression in pancreatic cancer tissues (53 samples) and Panc-1 human pancreatic cancer cells by immunohistochemistry, RT-PCR and western-blotting analyses. Also, immunohistochemistry of proliferating cell nuclear antigen (PCNA) was performed.

Effect of emodin on pancreatic fibrosis in rats.

Aim: To establish the rats model of chronic fibrosing pancreatitis and to prove the anti-fibrotic effect of emodin in chronic pancreatitis with fibrosis.

Methods: Fifty rats were randomly divided into five groups, 10 rats in each group. Trinitrobenzene sulfonic acid (TNBS) was infused into the pancreatic duct to induce chronic pancreatitis in rats (except for normal group).

[Effect of emodin on pancreatic fibrosis: experiment with rats].

Objective: To study the effect of emodin on pancreatic fibrosis and potential mechanism thereof.

Methods: Fifty SD rats were randomly divided into 5 equal groups: normal control group, model control group, low-dose emodin-treated group, mediate-dose emodin-treated group, and high-dose emodin-treated group. The rats of the latter 4 groups underwent infusion of trinitrobenzene sulfonic acid (TNBS) into the pancreatic duct so as to establish models of pancreatic fibrosis.

[Effect of selective cyclooxygenase-2 inhibitor celebrex on expression of vascular endothelial growth factor (VEGF) in pancreatic carcinoma].

Background & Objective: The previous study has identified that cyclooxygenase-2 (COX-2) may have a close relation with tumor genesis, particularly with digestive tract tumors, and its inhibitor can exert the chemoprevention role on carcinogenesis. This study was designed to investigate the effect of celebrex, a selective cyclooxygenase-2 inhibitor, on the expression of vascular endothelial growth factor (VEGF) in pancreatic carcinoma of xenografted nude mice induced by pancreatic carcinoma PC-3 cell lines.

Methods: The effect of celebrex on tumor growth was observed.

[Inhibition of angiogenesis in pancreatic carcinoma by cyclooxygenase-2 antisense oligodeoxynucleotides].

Objective: To investigate the effect of cyclooxygenase-2 antisense oligodeoxynucleotides (COX-2 AS-ODNs) on the angiogenesis in pancreatic carcinoma and to evaluate the intermediary effect of prostaglandin 2 in this process.

Methods: Specific targeting COX-2 AS-ODNs were designed and synthesized, and transfected into the PC3 human pancreatic carcinoma cells cultured in vitro. Fluorescence microscopy was used to observe the PC3 cells 0.