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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
04/2015, ISBN 0470673184, 459
Pancreatic Cancer, Cystic Neoplasms and Endocrine Tumors: Diagnosis and Management is a modern, expertly crafted and clinically focused guide to the diagnosis,... 
Diagnosis | Pancreas | Cancer | Neuroendocrine tumors
eBook
Nature Genetics, ISSN 1061-4036, 10/2013, Volume 45, Issue 10, pp. 1216 - 1220
Journal Article
Journal Article
Journal Article
Journal Article
Journal of Clinical Investigation, ISSN 0021-9738, 06/2012, Volume 122, Issue 6, pp. 2092 - 2103
Pancreatic ductal adenocarcinoma (PDAC) has the lowest survival rate of all cancers and shows remarkable resistance to cell stress. Nuclear protein 1 (Nupr1),... 
BREAST-CANCER | MEDICINE, RESEARCH & EXPERIMENTAL | ACTIVATION | METASTASIS | DUCTAL ADENOCARCINOMA | IEX-1 | GROWTH | GENE-EXPRESSION | KAPPA-B PATHWAY | P8 MESSENGER-RNA | PROGRESSION | Adenocarcinoma - pathology | Pancreatic Neoplasms - metabolism | Humans | Gene Expression Regulation, Neoplastic | Male | Neoplasm Proteins - metabolism | Oncogene Protein p21(ras) - metabolism | DNA-Binding Proteins - metabolism | Neoplasms, Experimental - pathology | Immediate-Early Proteins - metabolism | Adenocarcinoma - metabolism | Cell Transformation, Neoplastic - genetics | Mice, Mutant Strains | Gene Deletion | Neoplasms, Experimental - genetics | Apoptosis Regulatory Proteins - genetics | Female | Adenocarcinoma - genetics | Membrane Proteins - metabolism | Neoplasm Proteins - genetics | Transcription Factor RelB - genetics | Membrane Proteins - genetics | Pancreatic Neoplasms - pathology | Pancreatic Neoplasms - genetics | Signal Transduction - genetics | DNA-Binding Proteins - genetics | Cell Transformation, Neoplastic - metabolism | Apoptosis Regulatory Proteins - metabolism | Animals | Immediate-Early Proteins - genetics | Transcription Factor RelB - metabolism | Cell Line, Tumor | Mice | Neoplasms, Experimental - metabolism | Cell Transformation, Neoplastic - pathology | Apoptosis | Oncogene Protein p21(ras) - genetics | Cellular proteins | Pancreatic cancer | Development and progression | Genetic aspects | Properties | Risk factors | Index Medicus | Abridged Index Medicus
Journal Article
Pancreatology, ISSN 1424-3903, 2012, Volume 12, Issue 5, pp. e3 - e3
  Specifically, we detailed that IL-6 trans-signalling-dependent activation of Stat3/Socs3 is required to promote PanIN progression and pancreatic ductal... 
Endocrinology & Metabolism | Gastroenterology and Hepatology | Pancreas
Journal Article
PLoS ONE, ISSN 1932-6203, 03/2013, Volume 8, Issue 3, pp. e60529 - e60529
Background: Pancreatic neuritis is a histopathological hallmark of pancreatic neuropathy and correlates to abdominal neuropathic pain sensation in pancreatic... 
INFLAMMATION | MULTIDISCIPLINARY SCIENCES | INNERVATION | DEGRANULATION | SUBSTANCE-P | EXPRESSION | CORRELATE | IRRITABLE-BOWEL-SYNDROME | NERVE GROWTH-FACTOR | HYPERSENSITIVITY | PLASTICITY | Neuralgia - complications | Adenocarcinoma - pathology | Humans | Middle Aged | Receptor, PAR-1 - analysis | Male | Neuritis - pathology | Neuralgia - pathology | T-Lymphocytes, Cytotoxic - pathology | Neuralgia - immunology | Pancreas - innervation | Female | Macrophages - immunology | Pancreatitis, Chronic - immunology | T-Lymphocytes, Cytotoxic - immunology | Mast Cells - immunology | Macrophages - pathology | Adenocarcinoma - immunology | Pancreatic Neoplasms - pathology | Pancreas - pathology | Pancreas - immunology | Adenocarcinoma - complications | Pancreatitis, Chronic - pathology | Neuritis - complications | Neuritis - immunology | Pancreatitis, Chronic - complications | Mast Cells - pathology | Pancreatic Neoplasms - immunology | Receptor, PAR-2 - analysis | Aged | Pancreatic Neoplasms - complications | Proteases | Lymphocytes | Pancreatic cancer | Nerves | Pancreatitis | Inflammation | Macrophages | Adenocarcinoma | CD8 antigen | Helper cells | Cytotoxicity | Lymphocytes T | Colorimetry | Neuropathy | CD45 antigen | Ethics | Enteric nervous system | Pain | Rodents | Surgery | Neuritis | Elastase | Lesions | Pancreas | Growth factors | Pain perception | Leukocytes (eosinophilic) | Hypersensitivity | Patients | CD4 antigen | Chymase | Beta cells | White blood cells | Lymphocytes B | CD20 antigen | Mast cells | Immunoreactivity | Tumors | Cancer | Eosinophils | Index Medicus
Journal Article
The Journal of Pathology, ISSN 0022-3417, 05/2019, Volume 248, Issue 1, pp. 6 - 8
Obesity and acute pancreatitis are both proinflammatory conditions. Importantly, obesity increases severity in acute pancreatitis by enhancing inflammation. In... 
NF‐κBIL‐6 | obesity | acute pancreatitis | PGC‐1α | NF-κBIL-6 | PGC-1α | ACTIVATION | PGC-1 alpha | ONCOLOGY | PATHOLOGY | NF-kappa BIL-6 | Wine | Obesity | Deregulation | Transcription | Pancreatitis | Inflammation | Pancreas | Glycoprotein gp130 | Index Medicus
Journal Article
by Klionsky, Daniel J and Abdelmohsen, Kotb and Abe, Akihisa and Abedin, Md Joynal and Abeliovich, Hagai and Acevedo Arozena, Abraham and Adachi, Hiroaki and Adams, Christopher M and Adams, Peter D and Adeli, Khosrow and Adhihetty, Peter J and Adler, Sharon G and Agam, Galila and Agarwal, Rajesh and Aghi, Manish K and Agnello, Maria and Agostinis, Patrizia and Aguilar, Patricia V and Aguirre-Ghiso, Julio and Airoldi, Edoardo M and Ait-Si-Ali, Slimane and Akematsu, Takahiko and Akporiaye, Emmanuel T and Al-Rubeai, Mohamed and Albaiceta, Guillermo M and Albanese, Chris and Albani, Diego and Albert, Matthew L and Aldudo, Jesus and Algül, Hana and Alirezaei, Mehrdad and Alloza, Iraide and Almasan, Alexandru and Almonte-Beceril, Maylin and Alnemri, Emad S and Alonso, Covadonga and Altan-Bonnet, Nihal and Altieri, Dario C and Alvarez, Silvia and Alvarez-Erviti, Lydia and Alves, Sandro and Amadoro, Giuseppina and Amano, Atsuo and Amantini, Consuelo and Ambrosio, Santiago and Amelio, Ivano and Amer, Amal O and Amessou, Mohamed and Amon, Angelika and An, Zhenyi and Anania, Frank A and Andersen, Stig U and Andley, Usha P and Andreadi, Catherine K and Andrieu-Abadie, Nathalie and Anel, Alberto and Ann, David K and Anoopkumar-Dukie, Shailendra and Antonioli, Manuela and Aoki, Hiroshi and Apostolova, Nadezda and Aquila, Saveria and Aquilano, Katia and Araki, Koichi and Arama, Eli and Aranda, Agustin and Araya, Jun and Arcaro, Alexandre and Arias, Esperanza and Arimoto, Hirokazu and Ariosa, Aileen R and Armstrong, Jane L and Arnould, Thierry and Arsov, Ivica and Asanuma, Katsuhiko and Askanas, Valerie and Asselin, Eric and Atarashi, Ryuichiro and Atherton, Sally S and Atkin, Julie D and Attardi, Laura D and Auberger, Patrick and Auburger, Georg and Aurelian, Laure and Autelli, Riccardo and Avagliano, Laura and Avantaggiati, Maria Laura and Avrahami, Limor and Awale, Suresh and Azad, Neelam and Bachetti, Tiziana and Backer, Jonathan M and Bae, Dong-Hun and Bae, Jae-sung and Bae, Ok-Nam and Bae, Soo Han and Baehrecke, Eric H and Baek, Seung-Hoon and Baghdiguian, Stephen and Bagniewska-Zadworna, Agnieszka and ... and Medicinska fakulteten and Region Östergötland and Linköpings universitet and Institutionen för klinisk och experimentell medicin and Diagnostikcentrum and Klinisk patologi och klinisk genetik and Institutionen för medicin och hälsa and Avdelningen för läkemedelsforskning and Avdelningen för cellbiologi
Autophagy, ISSN 1554-8627, 01/2016, Volume 12, Issue 1, pp. 1 - 222
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