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Literature DB >> 19867267

DATA CONCERNING THE ETIOLOGY AND PATHOLOGY OF HEMORRHAGIC NECROSIS OF THE PANCREAS (ACUTE HEMORRHAGIC PANCREATITIS).

E L Opie¹, J C Meakins.

Abstract

Entities: Disease

Year: 1909 PMID： 19867267 PMCID： PMC2124723 DOI： 10.1084/jem.11.4.561

Source DB: PubMed Journal: J Exp Med ISSN： 0022-1007 Impact factor: 14.307

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16 in total

1. The role of phospholipase A2 in pancreatic acinar cell injury.

Authors: A J Hietaranta; Z G Lászik; H J Aho; P T Kortesuo; T J Nevalainen
Journal: Int J Pancreatol Date: 1991-02

2. Deoxycholic acid inhibited proliferation and induced apoptosis and necrosis by regulating the activity of transcription factors in rat pancreatic acinar cell line AR42J.

Authors: Guixin Zhang; Jingwen Zhang; Dong Shang; Bing Qi; Hailong Chen
Journal: In Vitro Cell Dev Biol Anim Date: 2015-05-20 Impact factor: 2.416

3. Effective Reduction in High Ethanol Drinking by Semisynthetic Tetracycline Derivatives.

Authors: Peter J Syapin; Joseph M Martinez; David C Curtis; Patrick C Marquardt; Clayton L Allison; Jessica A Groot; Carol Baby; Yazan M Al-Hasan; Ismael Segura; Matthew J Scheible; Katy T Nicholson; Jose Luis Redondo; David R M Trotter; David S Edwards; Susan E Bergeson
Journal: Alcohol Clin Exp Res Date: 2016-11-14 Impact factor: 3.455

4. Bile acids induce pancreatic acinar cell injury and pancreatitis by activating calcineurin.

Authors: Kamaldeen A Muili; Dong Wang; Abrahim I Orabi; Sheharyar Sarwar; Yuhuan Luo; Tanveer A Javed; John F Eisses; Syeda M Mahmood; Shunqian Jin; Vijay P Singh; Meena Ananthanaravanan; George Perides; John A Williams; Jeffery D Molkentin; Sohail Z Husain
Journal: J Biol Chem Date: 2012-11-12 Impact factor: 5.157

5. Pancreatic acinar cell nuclear factor κB activation because of bile acid exposure is dependent on calcineurin.

Authors: Kamaldeen A Muili; Shunqian Jin; Abrahim I Orabi; John F Eisses; Tanveer A Javed; Tianming Le; Rita Bottino; Thotalla Jayaraman; Sohail Z Husain
Journal: J Biol Chem Date: 2013-06-06 Impact factor: 5.157

6. Small Gallstone Size and Delayed Cholecystectomy Increase the Risk of Recurrent Pancreatobiliary Complications After Resolved Acute Biliary Pancreatitis.

Authors: Sung Bum Kim; Tae Nyeun Kim; Hyun Hee Chung; Kook Hyun Kim
Journal: Dig Dis Sci Date: 2016-12-29 Impact factor: 3.199

DATA CONCERNING THE ETIOLOGY AND PATHOLOGY OF HEMORRHAGIC NECROSIS OF THE PANCREAS (ACUTE HEMORRHAGIC PANCREATITIS).

1. The role of phospholipase A2 in pancreatic acinar cell injury.

2. Deoxycholic acid inhibited proliferation and induced apoptosis and necrosis by regulating the activity of transcription factors in rat pancreatic acinar cell line AR42J.

3. Effective Reduction in High Ethanol Drinking by Semisynthetic Tetracycline Derivatives.

4. Bile acids induce pancreatic acinar cell injury and pancreatitis by activating calcineurin.

5. Pancreatic acinar cell nuclear factor κB activation because of bile acid exposure is dependent on calcineurin.

6. Small Gallstone Size and Delayed Cholecystectomy Increase the Risk of Recurrent Pancreatobiliary Complications After Resolved Acute Biliary Pancreatitis.

7. [Metabolic changes in a patient in the early phase of acute pancreatitis].

Review 8. The role of phospholipase A2 in human acute pancreatitis.

9. TRPV4 channel opening mediates pressure-induced pancreatitis initiated by Piezo1 activation.

10. Piezo1-mediated stellate cell activation causes pressure-induced pancreatic fibrosis in mice.