Disappearing portal venous gas in acute pancreatitis and small bowel ischemia

McNicholas, Daniel; Kelly, Michael E.; Das, Jeeban Paul; Bowden, Dermot; Murphy, Joe M.; Malone, Carmel

doi:10.1016/j.radcr.2017.01.006

Cited by 5 publications

(2 citation statements)

References 12 publications

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“…Biliary pathology and alcohol misuse typify the most typical patterns of AP aetiology, accounting for 40% and 22% of all cases of the condition, respectively. Furthermore, other risk factors associated with the condition include trauma, hypercholesterolaemia, iatrogenic procedures and other idiopathic causes . It is estimated that approximately 30% of all AP patients will be subject to severe attacks, which is indicative of a high mortality rate .…”

Section: Introductionmentioning

confidence: 99%

“…hypercholesterolaemia, iatrogenic procedures and other idiopathic causes. 4 It is estimated that approximately 30% of all AP patients will be subject to severe attacks, which is indicative of a high mortality rate. 5 Owing to both the high mortality rate and exorbitant medical costs associated with the treatment of the more severe cases of AP, treatment of AP remains a critical challenge to the field of gastroenterology.…”

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confidence: 99%

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Retracted: S100A9 gene silencing inhibits the release of pro‐inflammatory cytokines by blocking the IL‐17 signalling pathway in mice with acute pancreatitis

Wang

Shen

et al. 2018

J Cellular Molecular Medi

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The study aimed to investigate whether S100A9 gene silencing mediating the IL‐17 pathway affected the release of pro‐inflammatory cytokines in acute pancreatitis (AP). Kunming mice were assigned to the normal, AP, AP + negative control (NC), AP + shRNA, AP + IgG and AP + anti IL‐17 groups. ELISA was applied to measure expressions of AMY, LDH, CRP, TNF‐α, IL‐6 and IL‐8. The cells were distributed into the control, blank, NC, shRNA1 and shRNA2 groups. MTT assay, flow cytometry, RT‐qPCR and Western blotting were used to evaluate cell proliferation, cell cycle and apoptosis, and expressions of S100A9, TLR4, RAGE, IL‐17, HMGB1 and S100A12 in tissues and cells. Compared with the normal group, the AP group displayed increased expressions of AMY, LDH, CRP, TNFα, IL‐6, IL‐8, S100A9, TLR4, RAGE, IL‐17, HMGB1 and S100A12. The AP + shRNA and AP + anti IL‐17 groups exhibited an opposite trend. The in vivo results: Compare with the control group, the blank, NC, shRNA1 and shRNA2 groups demonstrated increased expressions of S100A9, TLR4, RAGE, IL‐17, HMGB1 and S100A12, as well as cell apoptosis and cells at the G1 phase, with reduced proliferation. Compared with the blank and NC groups, the shRNA1 and shRNA2 groups had declined expressions of S100A9, TLR4, RAGE, IL‐17, HMGB1 and S100A12, as well as cell apoptosis and cells at the G1 phase, with elevated proliferation. The results indicated that S100A9 gene silencing suppressed the release of pro‐inflammatory cytokines through blocking of the IL‐17 pathway in AP.

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Section: Introductionmentioning

confidence: 99%

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confidence: 99%