ial therapeutic targets for COVID-19. Severe burns are characterized by the magnitude and duration of the hypermetabolic response thereafter, and demarcated by the loss of lean body mass and catabolism of fat stores. The aim of the present study was to delineate the temporal and location-specific physiological changes to adipose depots and downstream consequences post-burn in a murine model of thermal injury. C57BL/6 mice were subjected to a 30% total body surface area burn and body mass, food intake, and tissue mass were monitored for various time points up until 60 days post-injury. Mitochondrial respirometry was performed using a Seahorse XF96 analyzer. https://www.selleckchem.com/products/elacestrant.html Lipolytic markers and browning markers were analyzed via Western blotting and histology. A severe burn results in a futile cycle of lipolysis and white adipose tissue (WAT) browning, the sequelae of which include fat catabolism, hepatomegaly, and loss of body mass despite increased food intake. A dynamic remodeling of epididymal WAT was observed with acute and chronic increases in lipolysis. time points up until 60 days post-injury. Mitochondrial respirometry was performed using a Seahorse XF96 analyzer. Lipolytic markers and browning markers were analyzed via Western blotting and histology. A severe burn results in a futile cycle of lipolysis and white adipose tissue (WAT) browning, the sequelae of which include fat catabolism, hepatomegaly, and loss of body mass despite increased food intake. A dynamic remodeling of epididymal WAT was observed with acute and chronic increases in lipolysis. Moreover, we demonstrate that pathological browning of inguinal WAT persists up to 60 days post-burn, highlighting the magnitude of the β-adrenergic response to thermal injury. Our data suggests that adipose depots have a heterogeneous response to burns and that therapeutic interventions targeting these physiological changes can improve outcomes. These data may also have implications for treating catabolic conditions such as cancer cachexia as well as developing treatments for obesity and type II diabetes. To investigate the feasibility and the value of using mitochondrial quality control (MQC)-related proteins as biomarkers in septic patients. The enrolled subjects were divided into four groups healthy control group (n = 30), ICU control group (n = 62), septic nonshock group (n = 40), and septic shock group (n = 94). Serum levels of peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), fission protein 1 (Fis1), mitofusin2 (Mfn2), and Parkin were measured by enzyme-linked immunosorbent assay (ELISA) at the time of enrollment for all groups. Clinical parameters and laboratory test results were also collected. The levels of MQC-related biomarkers between any two of the four groups were significantly different (P < 0.001 for all). The serum levels of PGC-1α, Mfn2, and Parkin were lowest in healthy individuals; the levels were dramatically higher in the ICU control group compared to the others, and they decreased progressively from the septic nonshock group to the septic shock group. However, the pattern for Fis1 was inverse; the more severe the condition was, the higher the level of Fis1. Moreover, there was moderate correlation between MQC-related biomarkers and the SOFA score (PGC-1α, r = -0.662; Fis1, r = 0.609; Mfn2, r = -0.677; Parkin, r = 0.-0.674, P < 0.001 for all). The serum levels of PGC-1α, Fis1, Mfn2, and Parkin were significantly correlated with organ dysfunction and reflected the disease progression and severity. The dynamic surveillance of these four biomarkers could be beneficial to predict outcome and guide treatment. The serum levels of PGC-1α, Fis1, Mfn2, and Parkin were significantly correlated with organ dysfunction and reflected the disease progression and severity. The dynamic surveillance of these four biomarkers could be beneficial to predict outcome and guide treatment. Damage associated molecular patterns (DAMPs) stimulate endothelial syndecan-1 shedding and neutrophil extracellular traps (NET) formation. The role of NETs in trauma and trauma-induced hypercoagulability is unknown. We hypothesized that trauma patients with accelerated thrombin generation would have increased NETosis and syndecan-1 levels. In this pilot study, we analyzed 50 citrated plasma samples from 30 trauma patients at 0 h (n = 22) and 6 h (n = 28) from time of injury (TOI) and 21 samples from healthy volunteers, for a total of 71 samples included in analysis. Thrombin generation was quantified using calibrated automated thrombogram (CAT) and reported as lag time (LT), peak height (PH), and time to peak (ttPeak). Nucleosome calibrated (H3NUC) and free histone standardized (H3Free) ELISAs were used to quantify NETs. Syndecan-1 levels were quantified by ELISA. Results are presented as median [interquartile range] and Spearman rank correlations. Plasma levels of H3NUC were increased in trauma patient generation kinetics early after injury. Our pilot study demonstrates that trauma patients have increased NETosis, measured by H3NUC and H3Free levels, increased syndecan-1 shedding, and accelerated thrombin generation kinetics early after injury. Sepsis is the leading cause of acute kidney injury (AKI) in critical care patients. A cornerstone of sepsis-associated AKI is dysregulated inflammation driven by excessive activation of Toll-like receptor 4 (TLR4) pathway. MUC1, a membrane bound mucin expressed in both epithelial tubular cells and renal macrophages, has been shown to be involved in the regulation of TLRs. Therefore we hypothesized that MUC1 could mitigate the renal inflammatory response to TLR4 activation. To test this hypothesis, we used a murine model of endotoxin-induced AKI by intraperitoneal injection of lipopolysaccharide (LPS). We showed that Muc1-/- mice have a more severe renal dysfunction, an increased activation of the tissular NF-kB pathway and secreted more pro inflammatory cytokines compare to Muc1+/+ mice. By flow cytometry, we observed that the proportion of M1 (pro-inflammatory) macrophages in the kidneys of Muc1-/- mice was significantly increased. In human and murine primary macrophages, we showed that MUC1 is only induced in M1 type macrophages and that macrophages derived from Muc1-/- mice secreted more pro-inflammatory cytokines.