Pressure reactivity index (PRx) and brain tissue oxygen (PbtO2) are associated with outcome in TBI. This study explores the relationship between PRx and PbtO2 in adult moderate/severe TBI. Using the Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) high resolution ICU sub-study cohort, we evaluated those patients with archived high-frequency digital intra-parenchymal ICP and PbtO2 monitoring data of a minimum of 6 hours in duration, and the presence of a 6 month Glasgow Outcome Scale -Extended (GOSE) score. Digital physiologic signals were processed for ICP, PbtO2 and pressure reactivity index (PRx), with the % time above/below defined thresholds determined. The duration of ICP, PbtO2 and PRx derangements was characterised. Associations with dichotomized 6-month GOSE (alive/dead, and favourable/unfavourable outcome; 4 or less = unfavourable), were assessed. A total of 43 patients were included. Severely impaired cerebrovascular reactivity was seen during elevatedygen, ICP, physiologic burden.Traumatic brain injury (TBI) is a leading cause of death and disability in people under 45. The hallmark secondary injury profile after TBI involves dynamic interactions between inflammatory and metabolic pathways including fatty acids. Omega-3 polyunsaturated fatty acids (PUFAs) such as docosahexaenoic acid (DHA) have been shown to provide neuroprotective benefits by minimizing neuroinflammation in rodents. However, these effects have been less conclusive in humans. We postulate genetic variants influencing PUFA metabolism in humans could contribute to these disparate findings. Therefore, we sought to (1) characterize the circulating PUFA response and (2) evaluate the impact of rs174537 on inflammation following TBI. A prospective, single-center, observational pilot study was conducted to collect blood samples from Level-1 trauma patients (N=130) on admission and 24 hours post-admission. Plasma was used to quantify PUFA levels and inflammatory cytokines. DNA was extracted and genotyped at rs174537. Associations between PUFAs and inflammatory cytokines were analyzed for all trauma cases and stratified by race (Caucasians only), TBI (TBI N=47; non-TBI=83) and rs174537 genotype (GG N=33, GT/TT N=44). TBI patients had higher plasma DHA levels compared to non-TBI at 24hrs post injury (p=0.013). The SNP rs174537 was associated with both PUFA levels and inflammatory cytokines (p less then 0.05). Specifically, TBI patients with GG genotype exhibited the highest plasma levels of DHA (1.33%) and IL-8 (121.5±43.3 pg/ml), which were in turn associated with poorer outcomes. These data illustrate the impact of rs174537 on the post-TBI response. Further work is needed to ascertain how this genetic variant directly influences inflammation following trauma.There is a need to improve the quality of donor liver from donation after circulatory death (DCD). The purpose of this study was to investigate the effects and mechanism of normothermic machine perfusion (NMP) combined with bone marrow mesenchymal stem cells (BMMSCs) on the oxidative stress and mitochondrial function in DCD livers. DCD livers were obtained, a rat NMP system was established, and BMMSCs were extracted and identified. The DCD livers were grouped by their preservation method Normal, static cold storage (SCS), NMP (P), and NMP combined with BMMSCs (PB), and the preservation time was up to 8 h. An IAR20 cell oxidative stress injury model was established in vitro by simulating DCD oxidative stress injury, and co-culturing with BMMSCs for 6 h. Compared with SCS group, after 6 h in vitro, the PB and P groups had significantly improved liver function and liver histological damage, reduced hepatocyte apoptosis and oxidative stress, improved hepatocyte mitochondrial damage, and increased mitochondrial membrane potential. These indicators were significantly better in the PB group than in the P group. BMMSCs significantly inhibited reactive oxygen species (ROS) release from the IAR20 cell oxidative stress model in vitro, ameliorated mitochondrial damage, and increased mitochondrial membrane potential level. BMMSCs also downregulated the JNK-NF-κB signaling pathway significantly in the IAR20 cell oxidative stress model and promoted AMPK activation. We verified that NMP combined with BMMSCs also played the same role in the PB group. NMP combined with BMMSCs could improve liver quality by relieving oxidative stress injury and improving mitochondrial function in rat DCD livers. The mechanism of protective role might involve inhibiting the JNK-NF-κB pathway to reduce oxidative stress and promote AMPK activation, thereby reducing mitochondrial damage and increase mitochondrial function.Mycotic aneurysm is a life-threatening disease often caused by Salmonella, Staphylococci and Streptococci species. Interestingly, Escherichia Coli (E. Coli) is described as a rare causative agent. We report the case of a patient who developed a mycotic aortic and ruptured left iliac aneurysm due to E. Coli. The patient developed a secondary aortic graft infection due to a mesenteric ischemia with fecal peritonitis. A literature overview of the current knowledge on mycotic aortic aneurysms specifically due to E. Coli is discussed including the clinical characteristics of patients, the management of the disease and the post-operative outcomes.The present study represents the first empirical investigation of the mechanisms – a Hostile-Helpless (HH) attachment and reflective functioning (RF) – through which childhood abuse and neglect (CA&N) experiences may impact a mother’s likelihood to commit filicide. The sample was comprised of 46 mentally ill mothers. Differences in attachment-derived risk variables between filicidal mothers (FM) and non-filicidal mothers (NFM) were also examined. FM (n = 23) reported lower RF, higher HH attachment, and a more severe history of CA&N, compared to NFM (n = 23), but did not differ on the severity of childhood experiences of loss of and/or separation from attachment figures. selleck compound Bayesian analysis indicated that the mediated effect of more severe CA&N on the likelihood of committing filicide through higher HH attachment was significantly amplified by lower RF. A developmental interpretation of filicide is proposed and clinical implications for prevention and attachment-based interventions with at-risk mother-child dyads are discussed.