Comparison of a Continuous Noninvasive Temperature to Monitor Core Temperature Measures During Targeted Temperature Management
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AbstractBackground: Temperature modulating devices (TMD) currently utilize core temperature measurements during targeted temperature management (TTM) that are currently limited to esophageal (Et), bladder (Bt), or rectal (Rt) temperatures. We assessed the ability of a continuous noninvasive temperature monitor to accurately approximate core temperature during TTM. Methods: All patients undergoing TTM using a gel pad surface TMD and an existing core temperature monitoring device were eligible for this study. Core and continuous noninvasive temperature monitoring values were simultaneously recorded for up to 72 h of TTM. The two sets of temperature data were downloaded from a clinical data acquisition storage system at 1-min intervals. The Bland–Altman method assessed agreement between the core and continuous noninvasive temperature monitor values, by measuring the mean difference (± 2 SD) between these values. Results: There were 20 subjects that underwent study between January 2018 and March 2018 (55% women, age: 57 ± 14 years old, BMI: 28.9 + 9.8 kg/m2, 100% mechanically ventilated). The comparison patient temperature source was predominantly esophageal (n = 10) followed by bladder (n = 5) or rectal (n = 5). There were a total of 999 h of paired patient temperature data from esophageal (50%), bladder (25%), and rectal (25%) temperatures. Bland–Altman analysis demonstrated good agreement with the superficial temperature monitor and core temperature measures in all patients overall, with a difference mean of 0.06 ± 0.39 C (P = 0.99) and no proportional bias noted (β =0.002, P = 0.917). Conclusions: Continuous noninvasive temperature monitoring is a suitable alternative method for assessing core temperature during TTM. Future studies should focus on developing connectivity with a continuous noninvasive temperature monitor to approximate core temperature during TTM.
KeywordContinuous noninvasive temperature monitoring
Targeted temperature management
Identifier to cite or link to this itemhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85087611884&doi=10.1007%2fs12028-020-01036-9&partnerID=40&md5=783cd4a4bf028d5390b8e5cdd7594ce8; http://hdl.handle.net/10713/13379
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Repression of TNFalpha gene activation at febrile range temperature through modification of recruitment of transcriptional regulatorsCooper, Zachary A.; Hasday, Jeffrey D. (2009)We have previously shown that exposure to febrile-range temperatures (FRT, 39.5-40°C) reduces lipopolysaccaride (LPS)-induced tumor necrosis factor-α (TNFα) expression, in part through the direct interaction of heat shock factor-1 (HSF-1) with the TNFα gene promoter. However, it is not known whether exposure to FRT also modifies other proximal LPS-induced signaling events or recruitment of transcriptional regulators to the TNFα promoter. Using HSF-1-null mice, we confirmed that HSF-1 is required for FRT-induced repression of TNFα in vitro by LPS-stimulated bone marrow derived macrophages and in vivo in mice challenged intratracheally with LPS. Exposing LPS-stimulated RAW 264.7 mouse macrophages to FRT reduced TNFα expression, while increasing interleukin (IL)-1β expression despite the two genes being regulated by the same MyD88-dependent pathway. Global activation of the three LPS induced signaling intermediates that lead to cytokine gene expression, ERK and p38 MAPKs and NFκB, was not affected by exposing RAW 264.7 cells to FRT as assessed by western blot analysis of ERK and p38 phosphorylation and analysis of NFκB activation by EMSA and reporter plasmid expression assays. However, chromatin immunoprecipitation (ChIP) analysis demonstrated that exposure to FRT reduced LPS-induced recruitment of NFκB-p65 to the TNFα promoter, while increasing its recruitment to the IL-1β promoter. An additional ChIP analysis shows that LPS stimulated a 90% increase in recruitment of Sp1 to the proximal TNFα promoter at 37�C, which was completely abrogated by exposure to FRT even though FRT exposure increased intranuclear Sp1 DNA-binding as measured by EMSA. LPS also stimulated recruitment of both Elk-1 and ATF-2 to the proximal promoter, but FRT exposure had no significant effect on this process. ChIP analysis of the 1452 bp TNFα 5'flanking sequence (-1300/+152) revealed no additional heat shock response elements (HSEs) and no effect of FRT on chromatin acetylation on this sequence. These data suggest that FRT exerts its effects on cytokine gene expression in a gene specific manner through downstream effects on promoter activation, rather than through proximal receptor activation/signaling events. In conclusion, we describe new mechanisms through which TNFα expression is reduced at FRT through gene-specific reduction of NFκB and Sp1 recruitment to the TNFα promoter.
Effects of Physiological Temperature Changes On Micro RNA Expression and Their Functional ConsequencesPotla, Ratnakar; Hasday, Jeffrey D.; 0000-0001-5712-271X (2015)Physiological changes in human core body temperature have important biological consequences for host response to infection, inflammation and survival. Work from our lab and others have shown that changes in temperature within clinically relevant range modify the expression of many chemokines, cytokines and other signaling molecules. Previous studies have focused on transcriptional regulation of temperature-dependent gene expression. In our present studies, we analyzed the mechanisms of temperature-dependent post transcriptional gene regulation by small non coding RNAs called micro RNAs (miRNAs). We found that exposure to clinically relevant hypothermia (32°C) within physiological range increased the expression of a surprisingly limited subset of miRNAs with some unusual characteristics. These miRNAs represent the passenger strands of miRNA duplex that are usually less abundant at 37°C. The same miRNAs tended to decrease at 39.5°C. Three of these miRNA targeted protein kinase C alpha (PKCα), a key player in cell cycle regulation. PKCα protein levels decreased with temperature and were rescued by miRNA inhibition at 32°C. The PKCα-dependent block of G1-S cell cycle transition was reversed at 32°C, and the effects of 32°C abrogated by miRNA inhibition. We further studied the effects of physiological temperature change on wnt signaling pathway, which contains several predicted targets of temperature-sensitive miRNAs. Exposure to 32°C reduced and exposure to 39.5°C increased wnt signaling as measured by wnt-dependent gene expression and a wnt-dependent reporter plasmid. Hypothermia reduced cell levels of the wnt-dependent transcription factor, TCF7 and this was reversed by miRNA inhibitors. The potential impact of these temperature changes on lung injury, repair, and fibrosis was evaluated by analyzing expression of genes involved in epithelial mesenchymal transition, which were reduced at 32°C and increased at 39.5°C. These genes, including collagen-1, TWIST1, N-cadherin, and MMP7 have all been shown to markers of human lung fibrosing diseases. These studies suggest that fever may worsen and hypothermia mitigate lung fibrosis and identifies a set of temperature-sensitive miRNAs as one potential mechanism.