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Turnbull Chris D. Stockley James A. Madathil Shyam Huq Syed S. A. Cooper Brendan G. Ali Asad Wharton Simon Stradling John R. Heitmar Rebekka 《Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie》2022,260(7):2129-2139
Graefe's Archive for Clinical and Experimental Ophthalmology - Retinal microvascular endothelial dysfunction is thought to be of importance in the development of ocular vascular diseases.... 相似文献
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Björn-Christian Link Emre F. Yekebas Dean Bogoevski Asad Kutup Gerhard Adam Jakob R. Izbicki Gerrit Krupski 《Journal of gastrointestinal surgery》2007,11(2):166-170
Symptomatic biliary leakage following major upper abdominal surgery is a severe complication resulting in increased morbidity
and mortality. Treatment options usually include either endoscopic intervention or surgical revision. These options may be
burdened by a high perioperative risk for the patient (e.g., patients with severe disease) or simply may not be possible (e.g.,
nonpreserved gastroduodenal passage). In the past, percutaneous transhepatic cholangiodrainage did only seem to be a viable
option for patients with dilated bile ducts. Here, we present our experience in a consecutive series of patients with symptomatic
biliary leakage following major upper abdominal surgery and without dilation of the biliary system that underwent percutaneous
transhepatic cholangiodrainage. Percutaneous transhepatic cholangiodrainage was feasible in 15 of 18 patients (83.3%). The
procedure was technically not possible in three patients (16.7%). In 10 of the 15 patients (66.6%) with feasible percutaneous
transhepatic cholangiodrainage, biliary leakage was definitely controlled without the need for surgical revision. Depending
on the experience with the interventional procedure, percutaneous transhepatic cholangiodrainage should be considered as an
alternative for treatment of symptomatic biliary leakage instead of immediate reoperation.
Presented at the Digestive Disease Week 2005 (DDW), Chicago, IL, May 14–19, 2005 (poster presentation). 相似文献
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Niyaz Ahmed Mahfooz Alam A Abdul Majeed S Asad Rahman Angel Cataldi Debby Cousins Seyed E Hasnain 《Infection, genetics and evolution》2003,2(3):193-199
Tuberculosis in seals is caused by a member of the Mycobacterium tuberculosis complex referred to as the 'seal bacillus'. Fluorescent amplified-fragment length polymorphism (FAFLP) analysis was applied to isolates from four Australian and six Argentinean seals and compared with FAFLP pattern for standard strains belonging to the M. tuberculosis complex. The FAFLP profiles derived from EcoRI/MseI restricted fragments of blind coded DNA samples differentiated the seal bacillus from other members of the M. tuberculosis complex. According to the phylogenetic analysis performed using FAFLP data, seal bacilli appear to have diverged significantly from other members of the M. tuberculosis complex. We describe the suitability of a panel of 19 highly polymorphic markers for rapid identification and comparative genomic analyses of the seal bacillus strains. It is likely that these bacilli got separated from the M. tuberculosis lineage as a result of different insertion deletion events occurring on a genome wide scale. Our analysis reveals that the seal bacillus and M. bovis are genetically related and therefore, might have originated from a common ancestor. Our data additionally support the hypothesis that seal bacillus occupies a unique taxonomic position within the M. tuberculosis complex. 相似文献
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Mian A Guenther M Finegold M Ng P Rodgers J Lee B 《Molecular genetics and metabolism》2005,84(3):278-288
The host immune response to intracellular transgenes delivered by helper-dependent (HDV) vs. first generation (FGV) adenoviral vectors has been relatively unstudied. Previous studies showed short-term correction of bovine and murine argininosuccinate synthetase (ASS) deficiency after first generation adenoviral-mediated liver gene therapy. To determine whether the host adaptive immune response against the intracellular transgene human ASS (hASS) contributed to loss of gene expression in this setting, the same vector (FGV-CAG-hASS) was injected into Rag-/- (immunodeficient) mice. As in wild-type C57BL/6 (B6) mice, Rag-/- mice also showed significant loss of hASS expression and vector by week 4 post-injection, with concomitant elevation of liver enzymes and disruption of liver architecture. Therefore, direct toxicity due to vector rather than adaptive immune response against hASS primarily accounted for loss of expression with FGVs. In contrast to hASS, beta-galactosidase is strongly immunogenic and activates the host adaptive immune response. Loss of transgene expression was observed in B6 mice with either a FGV or a HDV expressing beta-galactosidase. However, the drop in gene expression observed with the HDV was primarily due to the adaptive immune response, since both beta-galactosidase expression and vector genome were sustained in immunodeficient mice treated with HDV. As expected, with weakly immunogenic hASS, vector genome and hASS expression were sustained with a HDV in spite of ubiquitous expression of the transgene. Therefore, viral gene expression is a primary determinant of intermediate and chronic toxicities at day 3 and week 4 post-injection. However, even in the absence of viral gene expression, strongly immunogenic intracellular transgenes can stimulate clearance of transduced hepatocytes. 相似文献
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Pelin Sahlén Rapolas Spalinskas Samina Asad Kunal Das Mahapatra Pontus Höjer Anandashankar Anil Jesper Eisfeldt Ankit Srivastava Pernilla Nikamo Anaya Mukherjee Kyu-Han Kim Otto Bergman Mona Ståhle Enikö Sonkoly Andor Pivarcsi Carl-Fredrik Wahlgren Magnus Nordenskjöld Fulya Taylan Isabel Tapia-Páez 《The Journal of allergy and clinical immunology》2021,147(5):1742-1752
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