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Rescue from complications after pancreaticoduodenectomies at a low-volume Caribbean center:Value of tailored peri-pancreatectomy protocols

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World Journal of Gastrointestinal Surgery 2024年第3期16卷 681-688页

作者： Shamir O Cawich Elijah Dixon Parul J Shukla shailesh V Shrikhande Rahul R deshpande Fawwaz Mohammed Neil W Pearce Wesley Francis Shaneeta Johnson Johann Bujhawan Department of Surgery University of the West IndiesSt Augustine 000000Trinidad and Tobago Department of Surgery Faculty of MedicineUniversity of CalgaryCalgaryAlberta T2N2T9Canada Department of Surgery Weill Cornell Medical CollegeNew YorkNY 10065United States Department of Surgical Oncology Tata Memorial CenterHomi Bhabha National UniversityMumbai 400012India Department of Surgery Manchester Royal InfirmaryManchester M139WLUnited Kingdom University Surgical Unit Southampton General HospitalSouthampton SO166YDUnited Kingdom Department of Surgery University of the West IndiesNassau N-1184Bahamas Department of Surgery Morehouse School of MedicineAtlantaGA 30310United States Department of Surgery General Hospital in Port of SpainPort of Spain 000000Trinidad and Tobago

BACKGROUND Pancreaticoduodenectomy(PD)is a technically complex operation,with a re-latively high risk for *** ability to rescue patients from post-PD complications is as a recognized quality *** protocols were instituted at our low volume facility in the year *** To document the rate of rescue from post-PD complications with tailored protocols in place as a measure of *** A retrospective audit was performed to collect data from patients who experienced major post-PD complications at a low volume pancreatic surgery unit in Trinidad and Tobago between January 1,2013 and June 30,***-dardized definitions from the International Study Group of Pancreatic Surgery were used to define post-PD complications,and the modified Clavien-Dindo classification was used to classify post-PD *** Over the study period,113 patients at a mean age of 57.5 years(standard deviation[SD]±9.23;range:30-90;median:56)underwent PDs at this *** complications were recorded in 33(29.2%)patients at a mean age of 53.8 years(SD:±7.9).Twenty-nine(87.9%)patients who experienced major morbidity were salvaged after aggre-ssive treatment of their ***(3.5%)died from bleeding pseudoaneurysm(1),septic shock secondary to a bile leak(1),anastomotic leak(1),and myocardial infarction(1).There was a significantly greater salvage rate in patients with American Society of Anesthesiologists scores≤2(93.3%vs 25%;P=0.0024).CONCLUSION This paper adds to the growing body of evidence that volume alone should not be used as a marker of quality for patients requiring *** low volumes at our facility,we demonstrated that 87.9%of patients were rescued from major *** attributed this to several factors including development of rescue protocols,the competence of the pancreatic surgery teams and continuous,and adaptive learning by the entire institution,cul-minating in the development of tailored peri-pancreatectomy protoc

关键词： Pancreas Complication Rescue Failure Morbidity Mortality Pancreaticoduodenectomy

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APE/Ref-1激活Akt通路保护HUVECs免于去血清培养诱导的细胞凋亡

APE/Ref-1激活Akt通路保护HUVECs免于去血清培养诱导的细胞凋亡

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第八届全国生化药理学术讨论会暨第七届Servier奖颁奖大会会议

作者：刘艳霞 deshpande shailesh Jeon Byeong-hua Ozaki Michitaka 李学军 Irani Kaikobad 天津医科大学基础医学院药理学教研室约翰·霍普金斯大学医学院心脏科北京大学医学部基础医学院药理学系

目的:一种多功能蛋白,人类无嘌呤/无嘧啶核酸内切酶/氧化还原因子-1(APE/Ref-1)通过修复损伤的DNA和促进核转录因子-kB与DNA结合而减轻由氧化张力诱导产生的细胞凋亡。本文研究是否Ref-1通过激活Akt激酶途径促进细胞生存。方法:人脐静...

目的:一种多功能蛋白,人类无嘌呤/无嘧啶核酸内切酶/氧化还原因子-1(APE/Ref-1)通过修复损伤的DNA和促进核转录因子-kB与DNA结合而减轻由氧化张力诱导产生的细胞凋亡。本文研究是否Ref-1通过激活Akt激酶途径促进细胞生存。方法:人脐静脉内皮细胞(HUVECs)培养于内皮细胞生长培养基(EGM)中,用不含生长因子和血清的内皮细胞基本培养基(EBM)培养内皮细胞40小时诱导细胞凋亡。编码Ref-1、Akt和突变型Akt的重组腺病毒Ad Ref-1、Ad myr-Akt和Ad AA-Akt用于诱导细胞过度表达相应的蛋白。无插入

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APE/Ref-1激活Akt通路保护HUVECs免于去血清培养诱导的细胞凋亡

APE/Ref-1激活Akt通路保护HUVECs免于去血清培养诱导的细胞凋亡

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2003全国中青年药理学英文学术报告会

作者：刘艳霞 Qi Bing deshpande shailesh Jeon Byeong-hua Ozaki Michitaka 李学军 Irani Kaikobad 天津医科大学基础医学院药理学教研室约翰·霍普金斯大学医学院心脏科北京大学医学部基础医学院药理学系

目的:一种多功能蛋白,人类无嘌呤/无嘧啶核酸内切酶/氧化还原因子-1(APE/Ref-1)通过修复损伤的DNA和促进核转录因子-κB与DNA结合而减轻由氧化张力诱导产生的细胞凋亡。本文研究是否Ref-1通过激活Akt激酶途径促进细胞生存。方法:人脐静...

目的:一种多功能蛋白,人类无嘌呤/无嘧啶核酸内切酶/氧化还原因子-1(APE/Ref-1)通过修复损伤的DNA和促进核转录因子-κB与DNA结合而减轻由氧化张力诱导产生的细胞凋亡。本文研究是否Ref-1通过激活Akt激酶途径促进细胞生存。方法:人脐静脉内皮细胞(HUVECs)培养于内皮细胞生长培养基(EGM)中,用不含生长因子和血清的内皮细胞基本培养基(EBM)培养内皮细胞40小时诱导细胞凋亡。编码Ref-1、Akt和突变型Akt的重组腺病毒Ad Ref-1、Ad myr-Akt和Ad AA-Akt用于诱导细胞过度表达相应的蛋白。无插入基因的腺病毒Ad D1312用做对照。

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Rac1 regulates the release of Weibel-Palade Bodies in human aortic endothelial cells

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Chinese Medical Journal 2004年第8期117卷 1143-1150页

作者：杨水祥闫娟 shailesh S.deshpande Kaikobad Irani Charles J.Lowenstein Cardiovascular Center Tongren Hospital Capital University of Medical SciencesBeijing100730China Division of Cardiology Department of Medicine Department of PathologyJohns Hopkins UniversitySchool of MedicineBaltimoreMaryland 21205USA

Background The release of Weibel-Palade Bodies (WPB) is a form of endothelial cell activation But the signal transduction pathway leading to WPB release is not yet defined We hypothesized that small G-protein rac1 and reactive oxygen species (ROS) mediate the ligand induced release of Weibel-Palade Bodies Methods We tested this hypothesis by using wild-type and mutant adenoviral rac1 expression vectors, and by manipulating the production and destruction of superoxide and hydrogen peroxide in human aortic endothelial cells (HAEC) KH*2/5DResults Thrombin (1 0 Unit, 30 min) induced the increase of WPB release by 3 7-fold in HAEC, and that H 2O 2 (0 1 mmol/L, 30 min) induced by 4 5-fold These results correlated with thrombin-stimulated activation of rac-GTP binding activity by 3 5-fold, and increase of ROS production by 3 4-fold The dominant negative adenoviral rac-N17 gene transfer dramatically inhibited the release of WPB by 64 2% (control) and 77 3% (thrombin-stimulation), and decreased ROS production by 65 5% (control) and 83 6% (thrombin-stimulation) compared with non-infected cells, respectively Anti-oxidants, catalase and N-acetyl-cysteine significantly decreased the release of WPB by 34% and 79% in control cells, and further decreased by 63 6% and 46 7% in rac-N17 transferred cells compared with non-infected cells We also confirmed that rac1 was located upstream of ROS in the WPB release pathway KH*2/5DConclusions Small G-protein rac1 medicates ligand-induced release of Weibel-Palade Bodies in human aortic endothelial cells, and the signal pathway of WPB release is a rac1-dependent ROS regulating mechanism

关键词： Weibel-Palade Bodies von Willebrand factor P-selectin rac thrombin exocytosis reactive oxygen species

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