| 1 |
Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) [J]. JAMA, 2016, 315(8): 775-787.
|
| 2 |
Iwashyna TJ, Ely EW, Smith DM, et al. Long-term cognitive impairment and functional disability among survivors of severe sepsis [J].JAMA, 2010, 304(16): 1787.
|
| 3 |
Patel MB, Morandi A, Pandharipande PP. What′s new in post-ICU cognitive impairment? [J]. Intensive Care Med, 2015, 41(4): 708-711.
|
| 4 |
Boomer JS, To K, Chang KC, et al. Immunosuppression in patients who die of sepsis and multiple organ failure [J]. JAMA, 2011, 306(23): 2594.
|
| 5 |
Angus DC. The lingering consequences of sepsis: a hidden public health disaster? [J]. JAMA, 2010, 304(16): 1833.
|
| 6 |
Angus D, Yang LL, Kellum J, et al. Circulating high-mobility group box 1 (HMGB1) concentrations are elevated in both uncomplicated pneumonia and pneumonia with severe sepsis [J]. Crit Care Med, 2007, 35(4): 1061-1067.
|
| 7 |
Chavan SS, Huerta PT, Robbiati S, et al. HMGB1 mediates cognitive impairment in sepsis survivors [J]. Mol Med, 2012, 18(9): 930.
|
| 8 |
Goodwin GH, Johns EW. Isolation and characterization of two calf-thymus chromatin non-histone proteins with high contents of acidic and basic amino acids [J]. Eur J Biochem, 1973, 40(1): 215-219.
|
| 9 |
Huang W, Tang YL. HMGB1, a potent proinflammatory cytokine in sepsis [J]. Cytokine, 2010, 51(2): 119-126.
|
| 10 |
Wang Q, Zeng M, Wang W, et al. The HMGB1 acidic tail regulates HMGB1 DNA binding specificity by a unique mechanism [J]. Biochem Bioph Res Co, 2007, 360(1): 14-19.
|
| 11 |
Bagherpoor AJ, Dolezalova D, Barta T, et al. Properties of human embryonic stem cells and their differentiated derivatives depend on nonhistone DNA-Binding HMGB1 and HMGB2 proteins [J]. Stem Cells Dev, 2017, 26(5): 328-340.
|
| 12 |
Takeda T, Izumi H, Kitada S, et al. The combination of a nuclear HMGB1-positive and HMGB2-negative expression is potentially associated with a shortened survival in patients with pancreatic ductal adenocarcinoma [J]. Tumor Biol, 2014, 35(10): 10555-10569.
|
| 13 |
Wang H, Ward MF, Sama AE. Targeting HMGB1 in the treatment of sepsis [J]. Expert Opin Ther Tar, 2014, 18(3): 257.
|
| 14 |
Zheng S, Pan Y, Wang C, et al. HMGB1 turns renal tubular epithelial cells into inflammatory promoters by interacting with TLR4 during sepsis [J]. J Interf Cytok Res, 2016, 36(1): 9.
|
| 15 |
Fucikova J, Moserova I, Truxova I, et al. High hydrostatic pressure induces immunogenic cell death in human tumor cells [J]. Int J Cancer, 2014, 135(5): 1165-11677.
|
| 16 |
Stevens NE, Chapman MJ, Fraser CK, et al. Therapeutic targeting of HMGB1 during experimental sepsis modulates the inflammatory cytokine profile to one associated with improved clinical outcomes [J]. Sci Rep, 2017, 7(1): 5850.
|
| 17 |
Abdulmahdi W, Patel D, Rabadi MM, et al. HMGB1 redox during sepsis [J]. Redox Bio, 2017, 13(C): 600-607.
|
| 18 |
Scaffidi P, Misteli T, Bianchi ME, et al. Release of chromatin protein HMGB1 by necrotic cells triggers inflammation [J]. Nature, 2002, 418(6894): 191-195.
|
| 19 |
Lotze MT, Tracey KJ. High-mobility group box 1 protein (HMGB1): nuclear weapon in the immune arsenal [J]. Nat Rev Immunol, 2005, 5(4): 331-342.
|
| 20 |
Wang H, Bloom O, Zhang M, et al. HMG-1 as a Late Mediator of Endotoxin Lethality in Mice [J]. Science, 1999, 285(5425): 248-251.
|
| 21 |
Wang H, Yang H, Tracey KJ. Extracellular role of HMGB1 in inflammation and sepsis [J]. J Intern Med, 2004, 255(3): 320.
|
| 22 |
Lotze MT, Tracey KJ. High-mobility group box 1 protein (HMGB1): nuclear weapon in the immune arsenal [J]. Nat Rev Immunol, 2005, 5(4): 331.
|
| 23 |
任超, 李秀花, 许碧磊, 等. 中枢拮抗高迁移率族蛋白B1对脓毒症脑损伤的影响 [J]. 中华急诊医学杂志, 2016, 25(4): 433-438.
|
| 24 |
董宁, 姚咏明, 于燕, 等. 严重烧伤后高迁移率族蛋白B1的变化及其与脓毒症的关系 [J]. 中国医学科学院学报, 2007, 29(4): 466-470.
|
| 25 |
Shah BA, Padbury JF. Neonatal sepsis: An old problem with new insights [J]. Virulence, 2014, 5(1): 170.
|
| 26 |
Ivanov S, Dragoi AM, Wang X, et al. A novel role for HMGB1 in TLR9-mediated inflammatory responses to CpG-DNA [J]. Blood, 2007, 110(6): 1970.
|
| 27 |
Gao M, Ha T, Zhang X, et al. Toll-like receptor 3 plays a central role in cardiac dysfunction during polymicrobial sepsis [J]. Crit Care Med, 2012, 40(8): 2390.
|
| 28 |
Wang H, Ward MF, Sama AE. Targeting HMGB1 in the treatment of sepsis [J]. Expert Opin Ther Tar, 2014, 18(3): 257-268.
|
| 29 |
Lu B, Nakamura T, Inouye K, et al. Novel role of PKR in inflammasome activation and HMGB1 release [J]. Nature, 2012, 488(7413): 670.
|
| 30 |
Rendonmitchell B, Ochani M, Li J, et al. IFN-γ induces high mobility group box 1 protein release partly through a TNF-dependent mechanism [J]. J Immunol, 2003, 170(7): 3890-3897.
|
| 31 |
Lee SA, Man SK, Kim S, et al. The role of high mobility group box 1 in innate immunity [J]. Yonsei Med J, 2014, 55(5): 1165-1176.
|
| 32 |
Tian J, Avalos AM, Mao SY, et al. Toll-like receptor 9-dependent activation by DNA-containing immune complexes is mediated by HMGB1 and RAGE [J]. Nat Immunol, 2007, 8(5): 487-496.
|
| 33 |
Yu M, Wang H, Ding A, et al. HMGB1 signals through toll-like receptor (TLR) 4 and TLR2 [J]. Shock, 2006, 26(2): 174.
|
| 34 |
Cheng Y, Xiong J, Chen Q, et al. Hypoxia/reoxygenation-induced HMGB1 translocation and release promotes islet proinflammatory cytokine production and early islet graft failure through TLRs signaling [J]. Biochim biophys Acta, 2016, 1863(2): 354-364.
|
| 35 |
Lian YJ, Gong H, Wu TY, et al. Ds-HMGB1 and fr-HMGB induce depressive behavior through neuroinflammation in contrast to nonoxid-HMGB1 [J]. Brain Behav Immun, 2017, 59: 322.
|
| 36 |
Tian J, Dai H, Deng Y, et al. The effect of HMGB1 on sub-toxic chlorpyrifos exposure-induced neuroinflammation in amygdala of neonatal rats [J]. Toxicology, 2015, 338: 95-103.
|
| 37 |
Lee S, Nam Y, Koo JY, et al. A small molecule binding HMGB1 and HMGB2 inhibits microglia-mediated neuroinflammation [J]. Nat Chem Biol, 2014, 10(12): 1055.
|
| 38 |
Danielski LG, Giustina AD, Badawy M, et al. Brain barrier breakdown as a cause and consequence of neuroinflammation in sepsis [J]. Mol Neurobiol, 2018, 55(2): 1045-1053.
|
| 39 |
Esen F, Senturk E, Ozcan PE, et al. Intravenous immunoglobulins prevent the breakdown of the blood-brain barrier in experimentally induced sepsis [J]. Crit Care Med, 2010, 14(S1): P24.
|
| 40 |
Andersson U, Tracey KJ. Neural reflexes in inflammation and immunity [J]. J Exp Med, 2012, 209(6): 1057.
|
| 41 |
Tracey KJ. Physiology and immunology of the cholinergic antiinflammatory pathway [J]. J Clin Invest, 2007, 117(2): 289-296.
|
| 42 |
Michels M, Vieira AS, Vuolo F, et al. The role of microglia activation in the development of sepsis-induced long-term cognitive impairment [J]. Brain Behav Immun, 2015, 43(3): 54-59.
|
| 43 |
Moraes CA, Santos G, D′Avila JC, et al. Activated microglia-induced deficits in excitatory synapses through IL-1β: implications for cognitive impairment in sepsis [J]. Mol Neurobiol, 2015, 52(1): 653-663.
|
| 44 |
Agalave NM, Larsson M, Abdelmoaty S, et al. Spinal HMGB1 induces TLR4-mediated long-lasting hypersensitivity and glial activation and regulates pain-like behavior in experimental arthritis [J]. Pain®, 2014, 155(9): 1802-1813.
|
| 45 |
Gao HM, Zhou H, Zhang F, et al. HMGB1 acts on microglia Mac1 to mediate chronic neuroinflammation that drives progressive neurodegeneration [J]. J Neurosci, 2011, 31(3): 1081.
|
| 46 |
O′Connor KA, Hansen MK, Pugh CR, et al. Further characterization of high mobility group box 1 (HMGB1) as a proinflammatory cytokine: central nervous system effects [J]. Cytokine, 2003, 24(6): 254.
|
| 47 |
Kim S, Dede AJ, Hopkins RO, et al. Memory, scene construction, and the human hippocampus [J]. P Natl Acad Sci USA, 2015, 112(15): 4767-4772.
|
| 48 |
Olivieri R, Michels M, Pescador B, et al. The additive effect of aging on sepsis-induced cognitive impairment and neuroinflammation [J]. J Neuro Immunol, 2018, 314: 1-7.
|
| 49 |
Semmler A, Widmann CN, Okulla T, et al. Persistent cognitive impairment, hippocampal atrophy and EEG changes in sepsis survivors [J]. J Neurol Neurosurg Psychiatry, 2013, 84(1): 62-69.
|
| 50 |
Semmler A, Okulla T, Sastre M, et al. Systemic inflammation induces apoptosis with variable vulnerability of different brain regions [J]. J Chem Neuroanat, 2005, 30(2-3): 144.
|
| 51 |
Li Z, Li B, Zhu X, et al. Neuroprotective effects of anti-high-mobility group box 1 antibody in juvenile rat hippocampus after kainic acid-induced status epilepticus [J]. Neuroreport, 2013, 24(14): 785-790.
|