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| 1 | Heparin resistance in severe thermal injury:a prospective cohort study显示文摘Background:Low molecular-weight heparin(LMWH)is routinely administered to burn patients for thromboprophylaxis.Some studies have reported heparin resistance,yet the mechanism(s)and prevalence have not been systematically studied.We hypothesized that nucleosomes,composed of histone structures with associated DNA released from injured tissue and activated immune cells in the form of neutrophil extracellular traps(NETs or NETosis),neutralize LMWH resulting in suboptimal anticoagulation,assessed by reduction in anti-factor Xa activity.Methods:Blood was sampled from>15%total body surface area(TBSA)burn patients receiving LMWH on days 5,10 and 14.Peak anti-factor Xa(AFXa)activity,anti-thrombin(ATIII)activity,cellfree DNA(cfDNA)levels and nucleosome levels were measured.Mixed effects regression was adjusted for multiple confounders,including injury severity and ATIII activity,and was used to test the association between nucleosomes and AFXa.Results:A total of 30 patients with severe burns were included.Mean TBSA 43%(SD 17).Twentythree(77%)patients were affected by heparin resistance(defined by AFXa activity<0.2 IU/mL).Mean peak AFXa activity across samples was 0.18 IU/mL(SD 0.11).Mean ATIII was 81.9%activity(SD 20.4).Samples taken at higher LWMH doses were found to have significantly increased AFXa activity,though the effect was not observed at all doses,at 8000 IU no samples were heparin resistant.Nucleosome levels were negatively correlated with AFXa(r=−0.29,p=0.050)consistent with the hypothesis.The final model,with peak AFXa as the response variable,was adjusted for nucleosome levels(p=0.0453),ATIII activity(p=0.0053),LMWH dose pre-sample(p=0.0049),drug given(enoxaparin or tinzaparin)(p=0.03),and other confounders including severity of injury,age,gender,time point of sample.Conclusions:Heparin resistance is a prevalent issue in severe burns.Nucleosome levels were increased post-burn,and showed an inverse association with AFXa consistent with the hypothesis that they may interfere with the anticoagulant effect of heparin in vivo and contribute to heparin resistance.Accurate monitoring of AFXa activity with appropriate therapy escalation plans are recommended with dose adjustment following severe burn injury. | Liam D Cato Benjamin Bailiff Joshua Price Christos Ermogeneous Jon Hazeldine William Lester Gillian Lowe Christopher Wearn Jonathan RB Bishop Janet M Lord Naiem Moiemen Paul Harrison | 2021 | Burns & Trauma2021，9，1： | 3 |
| 2 | Inflammation, Telomere Length, and Grip Strength: A 10-year Longitudinal Study显示文摘 | Daniel Baylis Georgia Ntani Mark H. Edwards Holly E. Syddall David B. Bartlett Elaine M. Dennison Carmen Martin-Ruiz Thomas Zglinicki Diana Kuh Janet M. Lord Avan Aihie Sayer Cyrus Cooper | 2014 | Calcified Tissue International2014，，1： | 1 |
| 3 | Bile Acids Reduce the Apoptosis-Inducing Effects of Sodium Butyrate on Human Colon Adenoma (AA/C1) Cells: Implications for Colon Carcinogenesis显示文摘 | Lorna McMillan Stephen Butcher Yvonne Wallis John P. Neoptolemos Janet M. Lord | 2000 | Biochemical and Biophysical Research Communications2000，，1： | 1 |
| 4 | Dehydroepiandrosterone:a potential therapeutic agent in the treatment and rehabilitation of the traumatically injured patient显示文摘Severe injuries are the major cause of death in those aged under 40,mainly due to road traffic collisions.Endocrine,metabolic and immune pathways respond to limit the tissue damage sustained and initiate wound healing,repair and regeneration mechanisms.However,depending on age and sex,the response to injury and patient prognosis differ significantly.Glucocorticoids are catabolic and immunosuppressive and are produced as part of the stress response to injury leading to an intra-adrenal shift in steroid biosynthesis at the expense of the anabolic and immune enhancing steroid hormone dehydroepiandrosterone(DHEA)and its sulphated metabolite dehydroepiandrosterone sulphate(DHEAS).The balance of these steroids after injury appears to influence outcomes in injured humans,with high cortisol:DHEAS ratio associated with increased morbidity and mortality.Animal models of trauma,sepsis,wound healing,neuroprotection and burns have all shown a reduction in proinflammatory cytokines,improved survival and increased resistance to pathological challenges with DHEA supplementation.Human supplementation studies,which have focused on post-menopausal females,older adults,or adrenal insufficiency have shown that restoring the cortisol:DHEAS ratio improves wound healing,mood,bone remodelling and psychological well-being.Currently,there are no DHEA or DHEAS supplementation studies in trauma patients,but we review here the evidence for this potential therapeutic agent in the treatment and rehabilitation of the severely injured patient. | Conor Bentley Jon Hazeldine Carolyn Greig Janet Lord Mark Foster | 2019 | Burns & Trauma2019，7，1： | 1 |
| 5 | Biliary Sterol Secretion Is Not Required for Macrophage Reverse Cholesterol Transport显示文摘 | Ryan E. Temel Janet K. Sawyer Liqing Yu Caleb Lord Chiara Degirolamo Allison McDaniel Stephanie Marshall Nanping Wang Ramesh Shah Lawrence L. Rudel J. Mark Brown | 2010 | Cell Metabolism2010，，1： | 1 |
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