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Konstantinos Vasiliadis,Elena Moschou,Sofia Papaioannou,Panagiotis Tzitzis,Albion Totsi,Stamatia Dimou,Eleni Lazaridou,Dimitrios Kapetanos,Christos Papavasiliou 한국간담췌외과학회 2020 Annals of hepato-biliary-pancreatic surgery Vol.24 No.2
A typical bile duct branching patterns represent one of the major causes of bile duct injury (BDI) during laparoscopic cholecystectomy (LC). The most common classified variations of bile duct branching, involve the right posterior sectoral duct (RPSD) and its joining with the right anterior or left hepatic duct. Variant bile duct anatomy can rarely be extremely complex and unclassified. This report describes an extremely rare case of an isolated injury to an aberrant right hepatic duct formed by the joining of ducts from segments V, VII, and VIII draining into the cystic duct (cysticohepatic duct) during LC, associated with an inferior RPSD opening to left hepatic duct. Detailed evaluation of both endoscopic and magnetic cholangiograms established the diagnosis. Bile duct injury was subsequently managed surgically by a demanding Roux-en-Y hepaticojejunostomy. This extremely rare case aims to serve as a useful reminder of the consistent inconsistency of biliary anatomy, alerting surgeons to beware of variant bile duct branching patterns during open or LC that constitute a dreadful pitfall for severe and life-threatening bile duct injuries.
An NADPH-Oxidase/Polyamine Oxidase Feedback Loop Controls Oxidative Burst Under Salinity
Gé,mes, Katalin,Kim, Yu Jung,Park, Ky Young,Moschou, Panagiotis N.,Andronis, Efthimios,Valassaki, Chryssanthi,Roussis, Andreas,Roubelakis-Angelakis, Kalliopi A. American Society of Plant Biologists 2016 Plant Physiology Vol.172 No.3
<P>The apoplastic polyamine oxidase (PAO) catalyzes the oxidation of the higher polyamines spermidine and spermine, contributing to hydrogen peroxide (H2O2) accumulation. However, it is yet unclear whether apoplastic PAO is part of a network that coordinates the accumulation of reactive oxygen species (ROS) under salinity or if it acts independently. Here, we unravel that NADPH oxidase and apoplastic PAO cooperate to control the accumulation of H2O2 and superoxides (O-2(center dot-)) in tobacco (Nicotiana tabacum). To examine to what extent apoplastic PAO constitutes part of a ROS-generating network, we examined ROS accumulation in guard cells of plants overexpressing or down-regulating apoplastic PAO (lines S2.2 and A2, respectively) or down-regulating NADPH oxidase (line AS-NtRbohD/F). The H2O2-specific probe benzene sulfonyl-H2O2 showed that, under salinity, H2O2 increased in S2.2 and decreased in A2 compared with the wild type. Surprisingly, the O-2(center dot-)-specific probe benzene sulfonyl-So showed that O-2(center dot-) levels correlated positively with that of apoplastic PAO (i.e. showed high and low levels in S2.2 and A2, respectively). By using AS-NtRbohD/F lines and a pharmacological approach, we could show that H2O2 and O-2(center dot-) accumulation at the onset of salinity stress was dependent on NADPH oxidase, indicating that NADPH oxidase is upstream of apoplastic PAO. Our results suggest that NADPH oxidase and the apoplastic PAO form a feed-forward ROS amplification loop, which impinges on oxidative state and culminates in the execution of programmed cell death. We propose that the PAO/NADPH oxidase loop is a central hub in the plethora of responses controlling salt stress tolerance, with potential functions extending beyond stress tolerance.</P>