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Cancer Research, ISSN 0008-5472, 08/2016, Volume 76, Issue 15 Supplement, pp. IA22 - IA22
Journal Article
Journal Article
Gastroenterology, ISSN 0016-5085, 12/2013, Volume 145, Issue 6, pp. 1480 - 1481
Journal Article
Gastroenterology, ISSN 0016-5085, 12/2013, Volume 145, Issue 6, p. 1480
Journal Article
Gastroenterology, ISSN 0016-5085, 12/2013, Volume 145, Issue 6, pp. 1480 - 1481
Journal Article
Gastroenterology, ISSN 0016-5085, 2013, Volume 145, Issue 6, pp. 1480 - 1481
Journal Article
Gastroenterology, ISSN 0016-5085, 2013, Volume 145, Issue 6, pp. 1480 - 1481
Journal Article
American Journal of Physiology - Cell Physiology, ISSN 0363-6143, 11/2009, Volume 297, Issue 5, pp. 1146 - 1156
Neuronal nitric oxide synthase (nNOS)-derived nitric oxide (NO) acts as a neurotransmitter and intracellular signaling molecule in the central and peripheral... 
Phosphatidylinositol 3-kinase/Akt signaling | DAX1 | Neuronal nitric oxide synthase | PHYSIOLOGY | NITRIC-OXIDE SYNTHASE | PHOSPHOINOSITIDE 3-KINASE/AKT PATHWAY | PANCREATIC-CANCER | neuronal nitric oxide synthase | CELL BIOLOGY | NUCLEAR RECEPTOR DAX1 | SIGNALING PATHWAY | MOUSE MODEL | GENE-EXPRESSION | TRANSCRIPTION FACTOR | NONGENOMIC ACTIONS | phosphatidylinositol 3-kinase/Akt signaling | NEURONAL NO SYNTHASE | Immunoprecipitation | Humans | Nitric Oxide Synthase Type I - biosynthesis | Phosphatidylinositol 3-Kinases - metabolism | DNA-Binding Proteins - metabolism | Transfection | DAX-1 Orphan Nuclear Receptor | Phosphatidylinositol 3-Kinases - drug effects | Antineoplastic Agents - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Repressor Proteins - metabolism | Tretinoin - pharmacology | Receptors, Retinoic Acid - drug effects | Gene Expression | DNA-Binding Proteins - drug effects | Gene Expression Regulation - physiology | Receptors, Retinoic Acid - metabolism | Reverse Transcriptase Polymerase Chain Reaction | Blotting, Western | Gene Expression Regulation - drug effects | Signal Transduction - drug effects | Cell Line, Tumor | Repressor Proteins - drug effects | Signal Transduction - physiology | Neuroblastoma - metabolism | Nitric Oxide Synthase Type I - drug effects | Proto-Oncogene Proteins c-akt - drug effects | Analysis | Physiological aspects | Cellular signal transduction | Research | Neuroblastoma | Gene expression | Protein kinases | Risk factors | Signal transduction | Protein synthesis | Nitric oxide | Physiology | Kinases | Cells | Index Medicus
Journal Article
Gut, ISSN 0017-5749, 11/2016, Volume 65, Issue 11, pp. 1780 - U6
  PC treatment is further complicated by a dense tumour stroma and low vessel density, leading to impaired drug delivery and high adverse effects of systemic... 
GASTROENTEROLOGY & HEPATOLOGY | Chemotherapy | Transplants & implants | Pancreatic cancer | Cell cycle | Clinical trials | Lipids | Kinases | Cancer therapies | Nanotechnology | Tumors | Index Medicus | Abridged Index Medicus
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 03/2013, Volume 123, Issue 3, pp. 1019 - 1031
Acute lung injury (ALI) is an inflammatory disease with a high mortality rate. Although typically seen in individuals with sepsis, ALI is also a major... 
C-REACTIVE PROTEIN | INFLAMMATORY-RESPONSE | MEDICINE, RESEARCH & EXPERIMENTAL | APOPTOSIS | Acute lung injury (ALI) is an inflammatory disease with a high mortality rate. Although typically seen in individuals with sepsis | of STAT3 and production of the neutrophil attractant CXCL1 in pancreatic acinar cells. Examination of human samples revealed expression of IL-6 in combination with soluble IL-6 receptor was a reliable predictor of ALI in SAP. These results demonstrate that IL-6 trans-signaling is an essential mediator of ALI in SAP across | INTERLEUKIN-6 | RESPIRATORY-DISTRESS-SYNDROME | PREDICTION | species and suggest that therapeutic inhibition of IL-6 may prevent SAP-associated ALI | ACUTE-PHASE RESPONSE | ALI is also a major complication in severe acute pancreatitis (SAP). The pathophysiology of SAP-associated ALI is poorly understood, but elevated serum levels of IL-6 is a reliable marker for disease severity. Here, we used a mouse model of acute pancreatitis-associated (AP-associated) ALI to determine the role of IL-6 in ALI lethality. Il6-deficient mice had a lower death rate compared with wild-type mice with AP, while mice injected with IL-6 were more likely to develop lethal ALI. We found that inflammation-associated NF-kappa B induced myeloid cell secretion of IL-6, and the effects of secreted IL-6 were mediated by complexation with soluble IL-6 receptor, a process known as trans-signaling. IL-6 trans-signaling stimulated phosphorylation | BLOCKADE | INHIBITOR | SEVERITY | Phosphorylation | Humans | NF-kappa B - metabolism | Pancreatitis - complications | Receptors, Interleukin-8B - antagonists & inhibitors | Benzenesulfonates - pharmacology | Interleukin-6 - physiology | Pancreatitis - immunology | Acute Lung Injury - metabolism | Chemokine CXCL1 - metabolism | STAT3 Transcription Factor - metabolism | Acinar Cells - metabolism | Aminosalicylic Acids - pharmacology | Signal Transduction | Mice, Inbred C57BL | Pancreas - pathology | Mice, Transgenic | Acute Lung Injury - pathology | Interleukin-6 - secretion | Animals | Myeloid Cells - secretion | Receptors, Interleukin-8B - metabolism | Myeloid Cells - metabolism | Acute Lung Injury - immunology | Pancreatitis - pathology | Mice | Phenylurea Compounds - pharmacology | Protein Processing, Post-Translational | Pancreatitis - metabolism | STAT3 Transcription Factor - antagonists & inhibitors | Acute Lung Injury - etiology | Receptors, Interleukin-6 - metabolism | Lung diseases | Pancreatitis | Genetic aspects | Research | Health aspects | Risk factors | Interleukin-6 | Index Medicus | Abridged Index Medicus | Clinical Medicine | Medical and Health Sciences | Klinisk medicin | Medicin och hälsovetenskap | Surgery | Kirurgi
Journal Article
The Journal of Physiology, ISSN 0022-3751, 10/2015, Volume 593, Issue 20, pp. 4589 - 4601
Journal Article
Journal Article
Pancreatology, ISSN 1424-3903, 2017, Volume 17, Issue 3, pp. S2 - S2
The deletion of the 3-phosphoinositide dependent protein kinase 1 (Pdk1) entirely blocks the formation of precursor lesions and PDAC in a pancreatic cancer... 
Endocrinology & Metabolism | Gastroenterology and Hepatology | Pancreas transplantation | Signal transduction | Kinases | Pancreatic cancer
Journal Article
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