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排序方式: 共有1462条查询结果,搜索用时 15 毫秒
51.
Histamine reduces boron neutron capture therapy‐induced mucositis in an oral precancer model 下载免费PDF全文
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Stéphanie Lejeune Muriel Pichavant Ilka Engelmann Laurent Béghin Elodie Drumez Olivier Le Rouzic Rodrigue Dessein Stéphanie Rogeau Timothée Beke Gwenola Kervoaze Céline Delvart Héloïse Ducoin Guillaume Pouessel Armelle Le Mée Sophie Boileau Juliette Roussel Cécile Bonnel Clémence Mordacq Caroline Thumerelle Philippe Gosset Antoine Deschildre 《Pediatric allergy and immunology》2020,31(6):651-661
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Efstathios Kastritis Ashutosh Wechalekar Stefan Schönland Vaishali Sanchorawala Giampaolo Merlini Giovanni Palladini Monique Minnema Murielle Roussel Arnaud Jaccard Ute Hegenbart Shaji Kumar Maria T. Cibeira Joan Blade Meletios A. Dimopoulos 《British journal of haematology》2020,190(3):346-357
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-associated coronavirus disease 2019 (COVID-19) is primarily manifested as a respiratory tract infection, but may affect and cause complications in multiple organ systems (cardiovascular, gastrointestinal, kidneys, haematopoietic and immune systems), while no proven specific therapy exists. The challenges associated with COVID-19 are even greater for patients with light chain (AL) amyloidosis, a rare multisystemic disease affecting the heart, kidneys, liver, gastrointestinal and nervous system. Patients with AL amyloidosis may need to receive chemotherapy, which probably increases infection risk. Management of COVID-19 may be particularly challenging in patients with AL amyloidosis, who often present with cardiac dysfunction, nephrotic syndrome, neuropathy, low blood pressure and gastrointestinal symptoms. In addition, patients with AL amyloidosis may be more susceptible to toxicities of drugs used to manage COVID-19. Access to health care may be difficult or limited, diagnosis of AL amyloidosis may be delayed with detrimental consequences and treatment administration may need modification. Both patients and treating physicians need to adapt in a new reality. 相似文献
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Auphan-Anezin N Mazza C Guimezanes A Barrett-Wilt GA Montero-Julian F Roussel A Hunt DF Malissen B Schmitt-Verhulst AM 《European journal of immunology》2006,36(7):1856-1866
We have characterized three different programs of activation for alloreactive CD8 T cells expressing the BM3.3 TCR, their elicitation depending on the characteristics of the stimulating peptide/MHC complex. The high-affinity interaction between the TCR and the K(b)-associated endogenous peptide pBM1 (INFDFNTI) induced a complete differentiation program into effector cells correlated with sustained ERK activation. The K(bm8) variant elicited a partial activation program with delayed T cell proliferation, poor CTL activity and undetectable ERK phosphorylation; this resulted from a low-avidity interaction of TCR BM3.3 with a newly identified endogenous peptide, pBM8 (SQYYYNSL). Interestingly, mismatched pBM1/K(bm8) complexes induced a split response in BM3.3 T cells, with total reconstitution of T cell proliferation but defective generation of CTL activity that was correlated with strong but shortened ERK phosphorylation. Crystal structures highlight the molecular basis for the higher stability of pBM8/K(bm8) compared to pBM1/K(bm8) complexes that exist in two conformers. This study illustrates the importance of the stability of both peptide/MHC and peptide/MHC-TCR interactions for induction of sustained signaling required to induce optimal CTL effector functions. Subtle allelic structural variations, amplified by peptide selection, may thus orient distinct outcomes of alloreactive TCR-based therapies. 相似文献
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K. F. E. Lee B. Lu J. C. Roussel L. J. Murray‐Segal E. J. Salvaris S. J. Hodgkinson B. M. Hall A. J. F. d'Apice H. Gock 《American journal of transplantation》2012,12(9):2363-2372
Thrombosis and inflammation are major obstacles to successful pig‐to‐human solid organ xenotransplantation. A potential solution is genetic modification of the donor pig to overexpress molecules such as the endothelial protein C receptor (EPCR), which has anticoagulant, anti‐inflammatory and cytoprotective signaling properties. Transgenic mice expressing human EPCR (hEPCR) were generated and characterized to test this approach. hEPCR was expressed widely and its compatibility with the mouse protein C pathway was evident from the anticoagulant phenotype of the transgenic mice, which exhibited a prolonged tail bleeding time and resistance to collagen‐induced thrombosis. hEPCR mice were protected in a model of warm renal ischemia reperfusion injury compared to wild type (WT) littermates (mean serum creatinine 39.0 ± 2.3 μmol/L vs. 78.5 ± 10.0 μmol/L, p < 0.05; mean injury score 31 ± 7% vs. 56 ± 5%, p < 0.05). Heterotopic cardiac xenografts from hEPCR mice showed a small but significant prolongation of survival in C6‐deficient PVG rat recipients compared to WT grafts (median graft survival 6 vs. 5 days, p < 0.05), with less hemorrhage and edema in rejected transgenic grafts. These data indicate that it is possible to overexpress EPCR at a sufficient level to provide protection against transplant‐related thrombotic and inflammatory injury, without detrimental effects in the donor animal. 相似文献